TY  - JOUR
AU  - Zarić, Božidarka
AU  - Obradović, Milan M.
AU  - Trpković, Andreja
AU  - Banach, Maciej
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2020
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8811
AB  - The endothelium consists of a monolayer of Endothelial Cells (ECs) which form the inner cellular lining of veins, arteries, capillaries and lymphatic vessels. ECs interact with the blood and lymph. The endothelium fulfils functions such as vasodilatation, regulation of adhesion, infiltration of leukocytes, inhibition of platelet adhesion, vessel remodeling and lipoprotein metabolism. ECs synthesize and release compounds such as Nitric Oxide (NO), metabolites of arachidonic acid, Reactive Oxygen Species (ROS) and enzymes that degrade the extracellular matrix. Endothelial dysfunction represents a phenotype prone to atherogenesis and may be used as a marker of atherosclerotic risk. Such dysfunction includes impaired synthesis and availability of NO and an imbalance in the relative contribution of endothelial-derived relaxing factors and contracting factors such as endothelin-1 and angiotensin. This dysfunction appears before the earliest anatomic evidence of atherosclerosis and could be an important initial step in further development of atherosclerosis. Endothelial dysfunction was historically treated with vitamin C supplementation and L-arginine supplementation. Short term improvement of the expression of adhesion molecule and endothelial function during antioxidant therapy has been observed. Statins are used in the treatment of hyperlipidaemia, a risk factor for cardiovascular disease. Future studies should focus on identifying the mechanisms involved in the beneficial effects of statins on the endothelium. This may help develop drugs specifically aimed at endothelial dysfunction. © 2020 Bentham Science Publishers.
T2  - Current Medicinal Chemistry
T1  - Endothelial dysfunction in dyslipidaemia: Molecular mechanisms and clinical implications
VL  - 27
IS  - 7
SP  - 1021
EP  - 1040
DO  - 10.2174/0929867326666190903112146
ER  - 

@article{
author = "Zarić, Božidarka and Obradović, Milan M. and Trpković, Andreja and Banach, Maciej and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2020",
abstract = "The endothelium consists of a monolayer of Endothelial Cells (ECs) which form the inner cellular lining of veins, arteries, capillaries and lymphatic vessels. ECs interact with the blood and lymph. The endothelium fulfils functions such as vasodilatation, regulation of adhesion, infiltration of leukocytes, inhibition of platelet adhesion, vessel remodeling and lipoprotein metabolism. ECs synthesize and release compounds such as Nitric Oxide (NO), metabolites of arachidonic acid, Reactive Oxygen Species (ROS) and enzymes that degrade the extracellular matrix. Endothelial dysfunction represents a phenotype prone to atherogenesis and may be used as a marker of atherosclerotic risk. Such dysfunction includes impaired synthesis and availability of NO and an imbalance in the relative contribution of endothelial-derived relaxing factors and contracting factors such as endothelin-1 and angiotensin. This dysfunction appears before the earliest anatomic evidence of atherosclerosis and could be an important initial step in further development of atherosclerosis. Endothelial dysfunction was historically treated with vitamin C supplementation and L-arginine supplementation. Short term improvement of the expression of adhesion molecule and endothelial function during antioxidant therapy has been observed. Statins are used in the treatment of hyperlipidaemia, a risk factor for cardiovascular disease. Future studies should focus on identifying the mechanisms involved in the beneficial effects of statins on the endothelium. This may help develop drugs specifically aimed at endothelial dysfunction. © 2020 Bentham Science Publishers.",
journal = "Current Medicinal Chemistry",
title = "Endothelial dysfunction in dyslipidaemia: Molecular mechanisms and clinical implications",
volume = "27",
number = "7",
pages = "1021-1040",
doi = "10.2174/0929867326666190903112146"
}

Zarić, B., Obradović, M. M., Trpković, A., Banach, M., Mikhailidis, D. P.,& Isenović, E. R.. (2020). Endothelial dysfunction in dyslipidaemia: Molecular mechanisms and clinical implications. in Current Medicinal Chemistry, 27(7), 1021-1040.
https://doi.org/10.2174/0929867326666190903112146

Zarić B, Obradović MM, Trpković A, Banach M, Mikhailidis DP, Isenović ER. Endothelial dysfunction in dyslipidaemia: Molecular mechanisms and clinical implications. in Current Medicinal Chemistry. 2020;27(7):1021-1040.
doi:10.2174/0929867326666190903112146 .

Zarić, Božidarka, Obradović, Milan M., Trpković, Andreja, Banach, Maciej, Mikhailidis, Dimitri P., Isenović, Esma R., "Endothelial dysfunction in dyslipidaemia: Molecular mechanisms and clinical implications" in Current Medicinal Chemistry, 27, no. 7 (2020):1021-1040,
https://doi.org/10.2174/0929867326666190903112146 . .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Essack, Magbubah
AU  - Zafirović, Sonja
AU  - Sudar-Milovanović, Emina
AU  - Bajić, Vladan P.
AU  - Van Neste, Christophe
AU  - Trpković, Andreja
AU  - Stanimirović, Julijana
AU  - Bajić, Vladimir B.
AU  - Isenović, Esma R.
PY  - 2020
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8486
AB  - Redox control is lost when the antioxidant defense system cannot remove abnormally high concentrations of signaling molecules, such as reactive oxygen species (ROS). Chronically elevated levels of ROS cause oxidative stress that may eventually lead to cancer and cardiovascular and neurodegenerative diseases. In this review, we focus on redox effects in the vascular system. We pay close attention to the subcompartments of the vascular system (endothelium, smooth muscle cell layer) and give an overview of how redox changes influence those different compartments. We also review the core aspects of redox biology, cardiovascular physiology, and pathophysiology. Moreover, the topic-specific knowledgebase DES-RedoxVasc was used to develop two case studies, one focused on endothelial cells and the other on the vascular smooth muscle cells, as a starting point to possibly extend our knowledge of redox control in vascular biology. © 2019 The Authors. BioFactors published by Wiley Periodicals, Inc. on behalf of International Union of Biochemistry and Molecular Biology.
T2  - BioFactors
T1  - Redox control of vascular biology
VL  - 46
IS  - 2
SP  - 246
EP  - 262
DO  - 10.1002/biof.1559
ER  - 

@article{
author = "Obradović, Milan M. and Essack, Magbubah and Zafirović, Sonja and Sudar-Milovanović, Emina and Bajić, Vladan P. and Van Neste, Christophe and Trpković, Andreja and Stanimirović, Julijana and Bajić, Vladimir B. and Isenović, Esma R.",
year = "2020",
abstract = "Redox control is lost when the antioxidant defense system cannot remove abnormally high concentrations of signaling molecules, such as reactive oxygen species (ROS). Chronically elevated levels of ROS cause oxidative stress that may eventually lead to cancer and cardiovascular and neurodegenerative diseases. In this review, we focus on redox effects in the vascular system. We pay close attention to the subcompartments of the vascular system (endothelium, smooth muscle cell layer) and give an overview of how redox changes influence those different compartments. We also review the core aspects of redox biology, cardiovascular physiology, and pathophysiology. Moreover, the topic-specific knowledgebase DES-RedoxVasc was used to develop two case studies, one focused on endothelial cells and the other on the vascular smooth muscle cells, as a starting point to possibly extend our knowledge of redox control in vascular biology. © 2019 The Authors. BioFactors published by Wiley Periodicals, Inc. on behalf of International Union of Biochemistry and Molecular Biology.",
journal = "BioFactors",
title = "Redox control of vascular biology",
volume = "46",
number = "2",
pages = "246-262",
doi = "10.1002/biof.1559"
}

Obradović, M. M., Essack, M., Zafirović, S., Sudar-Milovanović, E., Bajić, V. P., Van Neste, C., Trpković, A., Stanimirović, J., Bajić, V. B.,& Isenović, E. R.. (2020). Redox control of vascular biology. in BioFactors, 46(2), 246-262.
https://doi.org/10.1002/biof.1559

Obradović MM, Essack M, Zafirović S, Sudar-Milovanović E, Bajić VP, Van Neste C, Trpković A, Stanimirović J, Bajić VB, Isenović ER. Redox control of vascular biology. in BioFactors. 2020;46(2):246-262.
doi:10.1002/biof.1559 .

Obradović, Milan M., Essack, Magbubah, Zafirović, Sonja, Sudar-Milovanović, Emina, Bajić, Vladan P., Van Neste, Christophe, Trpković, Andreja, Stanimirović, Julijana, Bajić, Vladimir B., Isenović, Esma R., "Redox control of vascular biology" in BioFactors, 46, no. 2 (2020):246-262,
https://doi.org/10.1002/biof.1559 . .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Zafirović, Sonja
AU  - Soskić, Sanja S.
AU  - Stanimirović, Julijana
AU  - Trpković, Andreja
AU  - Jevremović, Danimir P.
AU  - Isenović, Esma R.
PY  - 2019
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8483
AB  - Cardiovascular (CV) diseases are the most common health problems worldwide, with a permanent increase in incidence. Growing evidence underlines that insulin-like growth factor 1 (IGF-1) is a very important hormone responsible for normal CV system physiology. IGF-1 is an anabolic growth hormone, responsible for cell growth, differentiation, proliferation, and survival. Despite systemic effects, IGF-1 exerts a wide array of influences in the CV system affecting metabolic homeostasis, vasorelaxation, cardiac contractility and hypertrophy, autophagy, apoptosis, and antioxidative processes. The vasodilatory effect of IGF-1, is achieved through the regulation of the activity of endothelial nitric oxide synthase (eNOS) and, at least partly, through enhancing inducible NOS (iNOS) activity. Also, IGF-1 stimulates vascular relaxation through regulation of sodium/potassium-adenosine-triphosphatase. Numerous animal studies provided evidence of diverse influences of IGF-1 in the CV system such as vasorelaxation, anti-apoptotic and prosurvival effects. Human studies indicate that low serum levels of free or total IGF-1 contribute to an increased risk of CV and cerebrovascular disease. Large human trials aiming at finding clinical efficacy and outcome of IGF-1-related therapy are of great interest. We look forward to the development of new IGF 1 therapies with minor side effects. In this review, we discuss the latest literature data regarding the function of IGF-1 in the CV system in the physiological and pathophysiological conditions. © 2019 Bentham Science Publishers.
T2  - Current Pharmaceutical Design
T1  - Effects of IGF-1 on the cardiovascular system
VL  - 25
IS  - 35
SP  - 3715
EP  - 3725
DO  - 10.2174/1381612825666191106091507
ER  - 

@article{
author = "Obradović, Milan M. and Zafirović, Sonja and Soskić, Sanja S. and Stanimirović, Julijana and Trpković, Andreja and Jevremović, Danimir P. and Isenović, Esma R.",
year = "2019",
abstract = "Cardiovascular (CV) diseases are the most common health problems worldwide, with a permanent increase in incidence. Growing evidence underlines that insulin-like growth factor 1 (IGF-1) is a very important hormone responsible for normal CV system physiology. IGF-1 is an anabolic growth hormone, responsible for cell growth, differentiation, proliferation, and survival. Despite systemic effects, IGF-1 exerts a wide array of influences in the CV system affecting metabolic homeostasis, vasorelaxation, cardiac contractility and hypertrophy, autophagy, apoptosis, and antioxidative processes. The vasodilatory effect of IGF-1, is achieved through the regulation of the activity of endothelial nitric oxide synthase (eNOS) and, at least partly, through enhancing inducible NOS (iNOS) activity. Also, IGF-1 stimulates vascular relaxation through regulation of sodium/potassium-adenosine-triphosphatase. Numerous animal studies provided evidence of diverse influences of IGF-1 in the CV system such as vasorelaxation, anti-apoptotic and prosurvival effects. Human studies indicate that low serum levels of free or total IGF-1 contribute to an increased risk of CV and cerebrovascular disease. Large human trials aiming at finding clinical efficacy and outcome of IGF-1-related therapy are of great interest. We look forward to the development of new IGF 1 therapies with minor side effects. In this review, we discuss the latest literature data regarding the function of IGF-1 in the CV system in the physiological and pathophysiological conditions. © 2019 Bentham Science Publishers.",
journal = "Current Pharmaceutical Design",
title = "Effects of IGF-1 on the cardiovascular system",
volume = "25",
number = "35",
pages = "3715-3725",
doi = "10.2174/1381612825666191106091507"
}

Obradović, M. M., Zafirović, S., Soskić, S. S., Stanimirović, J., Trpković, A., Jevremović, D. P.,& Isenović, E. R.. (2019). Effects of IGF-1 on the cardiovascular system. in Current Pharmaceutical Design, 25(35), 3715-3725.
https://doi.org/10.2174/1381612825666191106091507

Obradović MM, Zafirović S, Soskić SS, Stanimirović J, Trpković A, Jevremović DP, Isenović ER. Effects of IGF-1 on the cardiovascular system. in Current Pharmaceutical Design. 2019;25(35):3715-3725.
doi:10.2174/1381612825666191106091507 .

Obradović, Milan M., Zafirović, Sonja, Soskić, Sanja S., Stanimirović, Julijana, Trpković, Andreja, Jevremović, Danimir P., Isenović, Esma R., "Effects of IGF-1 on the cardiovascular system" in Current Pharmaceutical Design, 25, no. 35 (2019):3715-3725,
https://doi.org/10.2174/1381612825666191106091507 . .

TY  - JOUR
AU  - Essack, Magbubah
AU  - Salhi, Adil
AU  - Stanimirović, Julijana
AU  - Tifratene, Faroug
AU  - Bin Raies, Arwa
AU  - Hungler, Arnaud
AU  - Uludag, Mahmut
AU  - Van Neste, Christophe
AU  - Trpković, Andreja
AU  - Bajić, Vladan P.
AU  - Bajić, Vladimir B.
AU  - Isenović, Esma R.
PY  - 2019
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8389
AB  - In cellular physiology and signaling, reactive oxygen species (ROS) play one of the most critical roles. ROS overproduction leads to cellular oxidative stress. This may lead to an irrecoverable imbalance of redox (oxidation-reduction reaction) function that deregulates redox homeostasis, which itself could lead to several diseases including neurodegenerative disease, cardiovascular disease, and cancers. In this study, we focus on the redox effects related to vascular systems in mammals. To support research in this domain, we developed an online knowledge base, DES-RedoxVasc, which enables exploration of information contained in the biomedical scientific literature. The DES-RedoxVasc system analyzed 233399 documents consisting of PubMed abstracts and PubMed Central full-text articles related to different aspects of redox biology in vascular systems. It allows researchers to explore enriched concepts from 28 curated thematic dictionaries, as well as literature-derived potential associations of pairs of such enriched concepts, where associations themselves are statistically enriched. For example, the system allows exploration of associations of pathways, diseases, mutations, genes/proteins, miRNAs, long ncRNAs, toxins, drugs, biological processes, molecular functions, etc. that allow for insights about different aspects of redox effects and control of processes related to the vascular system. Moreover, we deliver case studies about some existing or possibly novel knowledge regarding redox of vascular biology demonstrating the usefulness of DES-RedoxVasc. DES-RedoxVasc is the first compiled knowledge base using text mining for the exploration of this topic.
T2  - Oxidative Medicine and Cellular Longevity
T1  - Literature-Based Enrichment Insights into Redox Control of Vascular Biology
VL  - 2019
SP  - 1769437
DO  - 10.1155/2019/1769437
ER  - 

@article{
author = "Essack, Magbubah and Salhi, Adil and Stanimirović, Julijana and Tifratene, Faroug and Bin Raies, Arwa and Hungler, Arnaud and Uludag, Mahmut and Van Neste, Christophe and Trpković, Andreja and Bajić, Vladan P. and Bajić, Vladimir B. and Isenović, Esma R.",
year = "2019",
abstract = "In cellular physiology and signaling, reactive oxygen species (ROS) play one of the most critical roles. ROS overproduction leads to cellular oxidative stress. This may lead to an irrecoverable imbalance of redox (oxidation-reduction reaction) function that deregulates redox homeostasis, which itself could lead to several diseases including neurodegenerative disease, cardiovascular disease, and cancers. In this study, we focus on the redox effects related to vascular systems in mammals. To support research in this domain, we developed an online knowledge base, DES-RedoxVasc, which enables exploration of information contained in the biomedical scientific literature. The DES-RedoxVasc system analyzed 233399 documents consisting of PubMed abstracts and PubMed Central full-text articles related to different aspects of redox biology in vascular systems. It allows researchers to explore enriched concepts from 28 curated thematic dictionaries, as well as literature-derived potential associations of pairs of such enriched concepts, where associations themselves are statistically enriched. For example, the system allows exploration of associations of pathways, diseases, mutations, genes/proteins, miRNAs, long ncRNAs, toxins, drugs, biological processes, molecular functions, etc. that allow for insights about different aspects of redox effects and control of processes related to the vascular system. Moreover, we deliver case studies about some existing or possibly novel knowledge regarding redox of vascular biology demonstrating the usefulness of DES-RedoxVasc. DES-RedoxVasc is the first compiled knowledge base using text mining for the exploration of this topic.",
journal = "Oxidative Medicine and Cellular Longevity",
title = "Literature-Based Enrichment Insights into Redox Control of Vascular Biology",
volume = "2019",
pages = "1769437",
doi = "10.1155/2019/1769437"
}

Essack, M., Salhi, A., Stanimirović, J., Tifratene, F., Bin Raies, A., Hungler, A., Uludag, M., Van Neste, C., Trpković, A., Bajić, V. P., Bajić, V. B.,& Isenović, E. R.. (2019). Literature-Based Enrichment Insights into Redox Control of Vascular Biology. in Oxidative Medicine and Cellular Longevity, 2019, 1769437.
https://doi.org/10.1155/2019/1769437

Essack M, Salhi A, Stanimirović J, Tifratene F, Bin Raies A, Hungler A, Uludag M, Van Neste C, Trpković A, Bajić VP, Bajić VB, Isenović ER. Literature-Based Enrichment Insights into Redox Control of Vascular Biology. in Oxidative Medicine and Cellular Longevity. 2019;2019:1769437.
doi:10.1155/2019/1769437 .

Essack, Magbubah, Salhi, Adil, Stanimirović, Julijana, Tifratene, Faroug, Bin Raies, Arwa, Hungler, Arnaud, Uludag, Mahmut, Van Neste, Christophe, Trpković, Andreja, Bajić, Vladan P., Bajić, Vladimir B., Isenović, Esma R., "Literature-Based Enrichment Insights into Redox Control of Vascular Biology" in Oxidative Medicine and Cellular Longevity, 2019 (2019):1769437,
https://doi.org/10.1155/2019/1769437 . .

TY  - JOUR
AU  - Trpković, Andreja
AU  - Resanović, Ivana
AU  - Stanimirović, Julijana
AU  - Radak, Đorđe J.
AU  - Mousa, Shaker A.
AU  - Cenić-Milošević, Desanka
AU  - Jevremovic, Danimir
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/635
AB  - Atherosclerosis is a life-long illness that begins with risk factors, which in turn contribute to the development of subclinical disease, followed by the establishment of overt cardiovascular disease (CVD). Thrombotic-occlusive complications of atherosclerosis are among the most widespread and costly health problems. Oxidized low-density lipoprotein (OxLDL) plays an important role in atherogenesis by promoting an inflammatory environment and lipid deposition in the arterial wall. As cardiovascular events occur in individuals without common risk factors, there is a need for additional tools that may help in CVD risk assessment and management. The use of biomarkers has improved diagnostic, therapeutic and prognostic outcome in cardiovascular medicine. This review elaborates on the value of circulating OxLDL as a biomarker of CVD. Three enzyme-linked immunosorbent assays (4E6, DLH3 and E06) using murine monoclonal antibodies for determination of OxLDL blood levels have been developed. However, none of these assays are currently approved for routine clinical practice. We identified studies investigating OxLDL in CVD (measured by 4E6, DLH3 or E06 assay) by searching the PubMed database. Circulating OxLDL was found to be associated with all stages of atherosclerosis, from early atherogenesis to hypertension, coronary and peripheral arterial disease, acute coronary syndromes and ischemic cerebral infarction. The results of studies investigating the usefulness of OxLDL for CVD prediction were also summarized. Furthermore, OxLDL was found to be associated with pathologic conditions linked to CVD, including diabetes mellitus, obesity and metabolic syndrome (MetS). In addition, we have addressed the mechanisms by which OxLDL promotes atherogenesis, and the effects of antiatherogenic treatments on circulating OxLDL. Finally, we highlight the evidence suggesting that lipoprotein (a) [ Lp(a)] is the preferential carrier of oxidized phospholipids (OxPL) in human plasma. A strong association between OxPLapoB level (representing the content of OxPL on apolipoprotein B-100 particles, measured by E06 assay) and Lp(a) has been determined.
T2  - Critical Reviews in Clinical Laboratory Sciences
T1  - Oxidized low-density lipoprotein as a biomarker of cardiovascular diseases
VL  - 52
IS  - 2
SP  - 70
EP  - 85
DO  - 10.3109/10408363.2014.992063
ER  - 

@article{
author = "Trpković, Andreja and Resanović, Ivana and Stanimirović, Julijana and Radak, Đorđe J. and Mousa, Shaker A. and Cenić-Milošević, Desanka and Jevremovic, Danimir and Isenović, Esma R.",
year = "2015",
abstract = "Atherosclerosis is a life-long illness that begins with risk factors, which in turn contribute to the development of subclinical disease, followed by the establishment of overt cardiovascular disease (CVD). Thrombotic-occlusive complications of atherosclerosis are among the most widespread and costly health problems. Oxidized low-density lipoprotein (OxLDL) plays an important role in atherogenesis by promoting an inflammatory environment and lipid deposition in the arterial wall. As cardiovascular events occur in individuals without common risk factors, there is a need for additional tools that may help in CVD risk assessment and management. The use of biomarkers has improved diagnostic, therapeutic and prognostic outcome in cardiovascular medicine. This review elaborates on the value of circulating OxLDL as a biomarker of CVD. Three enzyme-linked immunosorbent assays (4E6, DLH3 and E06) using murine monoclonal antibodies for determination of OxLDL blood levels have been developed. However, none of these assays are currently approved for routine clinical practice. We identified studies investigating OxLDL in CVD (measured by 4E6, DLH3 or E06 assay) by searching the PubMed database. Circulating OxLDL was found to be associated with all stages of atherosclerosis, from early atherogenesis to hypertension, coronary and peripheral arterial disease, acute coronary syndromes and ischemic cerebral infarction. The results of studies investigating the usefulness of OxLDL for CVD prediction were also summarized. Furthermore, OxLDL was found to be associated with pathologic conditions linked to CVD, including diabetes mellitus, obesity and metabolic syndrome (MetS). In addition, we have addressed the mechanisms by which OxLDL promotes atherogenesis, and the effects of antiatherogenic treatments on circulating OxLDL. Finally, we highlight the evidence suggesting that lipoprotein (a) [ Lp(a)] is the preferential carrier of oxidized phospholipids (OxPL) in human plasma. A strong association between OxPLapoB level (representing the content of OxPL on apolipoprotein B-100 particles, measured by E06 assay) and Lp(a) has been determined.",
journal = "Critical Reviews in Clinical Laboratory Sciences",
title = "Oxidized low-density lipoprotein as a biomarker of cardiovascular diseases",
volume = "52",
number = "2",
pages = "70-85",
doi = "10.3109/10408363.2014.992063"
}

Trpković, A., Resanović, I., Stanimirović, J., Radak, Đ. J., Mousa, S. A., Cenić-Milošević, D., Jevremovic, D.,& Isenović, E. R.. (2015). Oxidized low-density lipoprotein as a biomarker of cardiovascular diseases. in Critical Reviews in Clinical Laboratory Sciences, 52(2), 70-85.
https://doi.org/10.3109/10408363.2014.992063

Trpković A, Resanović I, Stanimirović J, Radak ĐJ, Mousa SA, Cenić-Milošević D, Jevremovic D, Isenović ER. Oxidized low-density lipoprotein as a biomarker of cardiovascular diseases. in Critical Reviews in Clinical Laboratory Sciences. 2015;52(2):70-85.
doi:10.3109/10408363.2014.992063 .

Trpković, Andreja, Resanović, Ivana, Stanimirović, Julijana, Radak, Đorđe J., Mousa, Shaker A., Cenić-Milošević, Desanka, Jevremovic, Danimir, Isenović, Esma R., "Oxidized low-density lipoprotein as a biomarker of cardiovascular diseases" in Critical Reviews in Clinical Laboratory Sciences, 52, no. 2 (2015):70-85,
https://doi.org/10.3109/10408363.2014.992063 . .

TY  - JOUR
AU  - Trpković, Andreja
AU  - Stanimirović, Julijana
AU  - Rizzo, Manfredi
AU  - Resanović, Ivana
AU  - Soskić, Sanja S.
AU  - Jevremovic, Danimir
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/613
AB  - The assessment of cardiovascular risk and treatment of cardiovascular diseases are major public health issues worldwide. Inflammation is now recognized as a key regulatory process that links multiple risk factors for atherosclerosis. The substantial number of patients having cardiovascular events lack commonly established risk factors. The utility of high-sensitivity C-reactive protein (hsCRP), a circulating biomarker related to inflammation, may provide additional information in risk prediction. This review will consider the impact of hsCRP level on initiation of statin therapy.
T2  - Angiology
T1  - High-Sensitivity C-Reactive Protein and Statin Initiation
VL  - 66
IS  - 6
SP  - 503
EP  - 507
DO  - 10.1177/0003319714543000
ER  - 

@article{
author = "Trpković, Andreja and Stanimirović, Julijana and Rizzo, Manfredi and Resanović, Ivana and Soskić, Sanja S. and Jevremovic, Danimir and Isenović, Esma R.",
year = "2015",
abstract = "The assessment of cardiovascular risk and treatment of cardiovascular diseases are major public health issues worldwide. Inflammation is now recognized as a key regulatory process that links multiple risk factors for atherosclerosis. The substantial number of patients having cardiovascular events lack commonly established risk factors. The utility of high-sensitivity C-reactive protein (hsCRP), a circulating biomarker related to inflammation, may provide additional information in risk prediction. This review will consider the impact of hsCRP level on initiation of statin therapy.",
journal = "Angiology",
title = "High-Sensitivity C-Reactive Protein and Statin Initiation",
volume = "66",
number = "6",
pages = "503-507",
doi = "10.1177/0003319714543000"
}

Trpković, A., Stanimirović, J., Rizzo, M., Resanović, I., Soskić, S. S., Jevremovic, D.,& Isenović, E. R.. (2015). High-Sensitivity C-Reactive Protein and Statin Initiation. in Angiology, 66(6), 503-507.
https://doi.org/10.1177/0003319714543000

Trpković A, Stanimirović J, Rizzo M, Resanović I, Soskić SS, Jevremovic D, Isenović ER. High-Sensitivity C-Reactive Protein and Statin Initiation. in Angiology. 2015;66(6):503-507.
doi:10.1177/0003319714543000 .

Trpković, Andreja, Stanimirović, Julijana, Rizzo, Manfredi, Resanović, Ivana, Soskić, Sanja S., Jevremovic, Danimir, Isenović, Esma R., "High-Sensitivity C-Reactive Protein and Statin Initiation" in Angiology, 66, no. 6 (2015):503-507,
https://doi.org/10.1177/0003319714543000 . .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Trpković, Andreja
AU  - Bajić, Vladan P.
AU  - Soskić, Sanja S.
AU  - Jovanović, Aleksandra
AU  - Stanimirović, Julijana
AU  - Panic, Milos
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/281
AB  - C-reactive protein (CRP) is a marker of inflammation. Atherosclerosis is now recognized as inflammatory disease, and it seems that CRP directly contributes to atherogenesis. Oxidation of low-density lipoprotein (LDL) molecule increases the uptake of lipid products by macrophages leading to cholesterol accumulation and subsequent foam cell formation. The elevated levels of high sensitivity CRP (hsCRP) and oxidized LDL (OxLDL) in the blood were found to be associated with cardiovascular diseases (CVD). In this review, we highlighted the evidence that CRP and OxLDL are involved in interrelated (patho) physiological pathways. The findings on association between hsCRP and OxLDL in the clinical setting will be also summarized.
T2  - Clinical Chemistry and Laboratory Medicine
T1  - Interrelatedness between C-reactive protein and oxidized low-density lipoprotein
VL  - 53
IS  - 1
SP  - 29
EP  - 34
DO  - 10.1515/cclm-2014-0590
ER  - 

@article{
author = "Obradović, Milan M. and Trpković, Andreja and Bajić, Vladan P. and Soskić, Sanja S. and Jovanović, Aleksandra and Stanimirović, Julijana and Panic, Milos and Isenović, Esma R.",
year = "2015",
abstract = "C-reactive protein (CRP) is a marker of inflammation. Atherosclerosis is now recognized as inflammatory disease, and it seems that CRP directly contributes to atherogenesis. Oxidation of low-density lipoprotein (LDL) molecule increases the uptake of lipid products by macrophages leading to cholesterol accumulation and subsequent foam cell formation. The elevated levels of high sensitivity CRP (hsCRP) and oxidized LDL (OxLDL) in the blood were found to be associated with cardiovascular diseases (CVD). In this review, we highlighted the evidence that CRP and OxLDL are involved in interrelated (patho) physiological pathways. The findings on association between hsCRP and OxLDL in the clinical setting will be also summarized.",
journal = "Clinical Chemistry and Laboratory Medicine",
title = "Interrelatedness between C-reactive protein and oxidized low-density lipoprotein",
volume = "53",
number = "1",
pages = "29-34",
doi = "10.1515/cclm-2014-0590"
}

Obradović, M. M., Trpković, A., Bajić, V. P., Soskić, S. S., Jovanović, A., Stanimirović, J., Panic, M.,& Isenović, E. R.. (2015). Interrelatedness between C-reactive protein and oxidized low-density lipoprotein. in Clinical Chemistry and Laboratory Medicine, 53(1), 29-34.
https://doi.org/10.1515/cclm-2014-0590

Obradović MM, Trpković A, Bajić VP, Soskić SS, Jovanović A, Stanimirović J, Panic M, Isenović ER. Interrelatedness between C-reactive protein and oxidized low-density lipoprotein. in Clinical Chemistry and Laboratory Medicine. 2015;53(1):29-34.
doi:10.1515/cclm-2014-0590 .

Obradović, Milan M., Trpković, Andreja, Bajić, Vladan P., Soskić, Sanja S., Jovanović, Aleksandra, Stanimirović, Julijana, Panic, Milos, Isenović, Esma R., "Interrelatedness between C-reactive protein and oxidized low-density lipoprotein" in Clinical Chemistry and Laboratory Medicine, 53, no. 1 (2015):29-34,
https://doi.org/10.1515/cclm-2014-0590 . .

TY  - JOUR
AU  - Trpković, Andreja
AU  - Stanimirović, Julijana
AU  - Resanović, Ivana
AU  - Otasevic, Petar
AU  - Jevremovic, Danimir
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/312
AB  - It is now recognized that inflammatory processes regulate all stages of atherosclerosis, from disease initiation to thrombotic complications. C-reactive protein (CRP) is a plasmatic protein used as a general marker of inflammation. The high sensitivity C-reactive protein (hsCRP) refers to the measurement of CRP in blood samples using assays with sufficient sensitivity to quantify low (baseline) levels of this biomarker. Low-grade chronic inflammatory processes are linked to atherosclerosis and may be screened with the use of hsCRP, thus providing additional information in cardiovascular risk prediction. This review elaborates the role of CRP in atherogenesis and the value of hsCRP as a biomarker in cardiovascular risk prediction in both primary and secondary prevention setting.
T2  - Current Pharmaceutical Analysis
T1  - High Sensitivity C-reactive Protein and Cardiovascular Risk Prediction
VL  - 11
IS  - 1
SP  - 60
EP  - 65
DO  - 10.2174/1573412910666140822003911
ER  - 

@article{
author = "Trpković, Andreja and Stanimirović, Julijana and Resanović, Ivana and Otasevic, Petar and Jevremovic, Danimir and Radak, Đorđe J. and Isenović, Esma R.",
year = "2015",
abstract = "It is now recognized that inflammatory processes regulate all stages of atherosclerosis, from disease initiation to thrombotic complications. C-reactive protein (CRP) is a plasmatic protein used as a general marker of inflammation. The high sensitivity C-reactive protein (hsCRP) refers to the measurement of CRP in blood samples using assays with sufficient sensitivity to quantify low (baseline) levels of this biomarker. Low-grade chronic inflammatory processes are linked to atherosclerosis and may be screened with the use of hsCRP, thus providing additional information in cardiovascular risk prediction. This review elaborates the role of CRP in atherogenesis and the value of hsCRP as a biomarker in cardiovascular risk prediction in both primary and secondary prevention setting.",
journal = "Current Pharmaceutical Analysis",
title = "High Sensitivity C-reactive Protein and Cardiovascular Risk Prediction",
volume = "11",
number = "1",
pages = "60-65",
doi = "10.2174/1573412910666140822003911"
}

Trpković, A., Stanimirović, J., Resanović, I., Otasevic, P., Jevremovic, D., Radak, Đ. J.,& Isenović, E. R.. (2015). High Sensitivity C-reactive Protein and Cardiovascular Risk Prediction. in Current Pharmaceutical Analysis, 11(1), 60-65.
https://doi.org/10.2174/1573412910666140822003911

Trpković A, Stanimirović J, Resanović I, Otasevic P, Jevremovic D, Radak ĐJ, Isenović ER. High Sensitivity C-reactive Protein and Cardiovascular Risk Prediction. in Current Pharmaceutical Analysis. 2015;11(1):60-65.
doi:10.2174/1573412910666140822003911 .

Trpković, Andreja, Stanimirović, Julijana, Resanović, Ivana, Otasevic, Petar, Jevremovic, Danimir, Radak, Đorđe J., Isenović, Esma R., "High Sensitivity C-reactive Protein and Cardiovascular Risk Prediction" in Current Pharmaceutical Analysis, 11, no. 1 (2015):60-65,
https://doi.org/10.2174/1573412910666140822003911 . .

TY  - JOUR
AU  - Trpković, Andreja
AU  - Pekmezovic, M.
AU  - Barac, A.
AU  - Radović Crncević, L.
AU  - Arsenijević, V. Arsic
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5128
AB  - Recently, geographic variations in resistance to agents commonly used in the treatment of cryptococcosis have been reported. Therefore, the antifungal susceptibilities of 31 clinical isolates of Cryptococcus neoformans, collected in Serbia during 10-year period, were investigated. Strains were isolated from cerebrospinal fluid (n = 28) and blood (n = 3), from patients with AIDS (n = 26), lymphoma (n = 4) and kidney transplant recipient (n = 1). The minimal inhibitory concentrations (MICs) of amphotericin B, 5-fluorocytosine, fluconazole and itraconazole were determined by the E-test (R) method. The isolates were highly susceptible to amphotericin B (100% susceptibility at MIC LT 0.5 mu g/mL) and 5-fluorocytosine (87.1% susceptibility at MIC LT = 4 mu g/mL). Geometric mean MIC of amphotericin B and 5-fluorocytosine were 0.102 mu g/mL and 0.396 mu g/mL, respectively. Fluconazole exhibited the lowest activity in vitro (48.4% susceptibility at MIC LT = 8 mu g/mL) with a significant resistance rate. The activity of itraconazole was also decreased (48.4% susceptibility at MIC LT = 0.25 mu g/mL). The geometric mean MIC of fiuconazole stood at 15.14 mu g/mL and of itraconazole was 0.144 mu g/mL. Cross-resistance among azoles was not common (3.2%), but the parallel increase in fluconazole and itraconazole MIC has been observed (P LT 0.01). The low rate of susceptibility to fluconazole stresses the need for active antifungal surveillance of C. neoformans and of the corresponding data from different geographic regions. (C) 2012 Elsevier Masson SAS. All rights reserved.
T2  - Journal de Mycologie Medicale
T1  - In vitro antifungal activities of amphotericin B, 5-fluorocytosine, fluconazole and itraconazole against Cryptococcus neoformans isolated from cerebrospinal fluid and blood from patients in Serbia
VL  - 22
IS  - 3
SP  - 243
EP  - 248
DO  - 10.1016/j.mycmed.2012.06.002
ER  - 

@article{
author = "Trpković, Andreja and Pekmezovic, M. and Barac, A. and Radović Crncević, L. and Arsenijević, V. Arsic",
year = "2012",
abstract = "Recently, geographic variations in resistance to agents commonly used in the treatment of cryptococcosis have been reported. Therefore, the antifungal susceptibilities of 31 clinical isolates of Cryptococcus neoformans, collected in Serbia during 10-year period, were investigated. Strains were isolated from cerebrospinal fluid (n = 28) and blood (n = 3), from patients with AIDS (n = 26), lymphoma (n = 4) and kidney transplant recipient (n = 1). The minimal inhibitory concentrations (MICs) of amphotericin B, 5-fluorocytosine, fluconazole and itraconazole were determined by the E-test (R) method. The isolates were highly susceptible to amphotericin B (100% susceptibility at MIC LT 0.5 mu g/mL) and 5-fluorocytosine (87.1% susceptibility at MIC LT = 4 mu g/mL). Geometric mean MIC of amphotericin B and 5-fluorocytosine were 0.102 mu g/mL and 0.396 mu g/mL, respectively. Fluconazole exhibited the lowest activity in vitro (48.4% susceptibility at MIC LT = 8 mu g/mL) with a significant resistance rate. The activity of itraconazole was also decreased (48.4% susceptibility at MIC LT = 0.25 mu g/mL). The geometric mean MIC of fiuconazole stood at 15.14 mu g/mL and of itraconazole was 0.144 mu g/mL. Cross-resistance among azoles was not common (3.2%), but the parallel increase in fluconazole and itraconazole MIC has been observed (P LT 0.01). The low rate of susceptibility to fluconazole stresses the need for active antifungal surveillance of C. neoformans and of the corresponding data from different geographic regions. (C) 2012 Elsevier Masson SAS. All rights reserved.",
journal = "Journal de Mycologie Medicale",
title = "In vitro antifungal activities of amphotericin B, 5-fluorocytosine, fluconazole and itraconazole against Cryptococcus neoformans isolated from cerebrospinal fluid and blood from patients in Serbia",
volume = "22",
number = "3",
pages = "243-248",
doi = "10.1016/j.mycmed.2012.06.002"
}

Trpković, A., Pekmezovic, M., Barac, A., Radović Crncević, L.,& Arsenijević, V. A.. (2012). In vitro antifungal activities of amphotericin B, 5-fluorocytosine, fluconazole and itraconazole against Cryptococcus neoformans isolated from cerebrospinal fluid and blood from patients in Serbia. in Journal de Mycologie Medicale, 22(3), 243-248.
https://doi.org/10.1016/j.mycmed.2012.06.002

Trpković A, Pekmezovic M, Barac A, Radović Crncević L, Arsenijević VA. In vitro antifungal activities of amphotericin B, 5-fluorocytosine, fluconazole and itraconazole against Cryptococcus neoformans isolated from cerebrospinal fluid and blood from patients in Serbia. in Journal de Mycologie Medicale. 2012;22(3):243-248.
doi:10.1016/j.mycmed.2012.06.002 .

Trpković, Andreja, Pekmezovic, M., Barac, A., Radović Crncević, L., Arsenijević, V. Arsic, "In vitro antifungal activities of amphotericin B, 5-fluorocytosine, fluconazole and itraconazole against Cryptococcus neoformans isolated from cerebrospinal fluid and blood from patients in Serbia" in Journal de Mycologie Medicale, 22, no. 3 (2012):243-248,
https://doi.org/10.1016/j.mycmed.2012.06.002 . .

TY  - JOUR
AU  - Trpković, Andreja
AU  - Todorović-Marković, Biljana
AU  - Trajković, Vladimir S.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5156
AB  - The fullerene C-60, due to the physicochemical properties of its spherical cage-like molecule build exclusively from carbon atoms, is able to both scavenge and generate reactive oxygen species. While this unique dual property could be exploited in biomedicine, the low water solubility of C-60 hampers the investigation of its behavior in biological systems. The C-60 can be brought into water by solvent extraction, by complexation with surfactants/polymers, or by long-term stirring, yielding pristine (unmodified) fullerene suspensions. On the other hand, a modification of the C-60 core by the attachment of various functional groups results in the formation of water-soluble fullerene derivatives. Assessment of toxicity associated with C-60 preparations is of pivotal importance for their biomedical application as cytoprotective (antioxidant), cytotoxic (anticancer), or drug delivery agents. Moreover, the widespread industrial utilization of fullerenes may also have implications for human health. However, the alterations in physicochemical properties imposed by the utilization of different methods for C-60 solubilization profoundly influence toxicological effects of fullerene preparations, thus making the analysis of their potential therapeutic and environmental toxicity difficult. This review provides a comprehensive evaluation of the in vitro and in vivo toxicity of fullerenes, focusing on the comparison between pristine and derivatized C-60 preparations and the mechanisms of their toxicity to mammalian cells and tissues.
T2  - Archives of Toxicology
T1  - Toxicity of pristine versus functionalized fullerenes: mechanisms of cell damage and the role of oxidative stress
VL  - 86
IS  - 12
SP  - 1809
EP  - 1827
DO  - 10.1007/s00204-012-0859-6
ER  - 

@article{
author = "Trpković, Andreja and Todorović-Marković, Biljana and Trajković, Vladimir S.",
year = "2012",
abstract = "The fullerene C-60, due to the physicochemical properties of its spherical cage-like molecule build exclusively from carbon atoms, is able to both scavenge and generate reactive oxygen species. While this unique dual property could be exploited in biomedicine, the low water solubility of C-60 hampers the investigation of its behavior in biological systems. The C-60 can be brought into water by solvent extraction, by complexation with surfactants/polymers, or by long-term stirring, yielding pristine (unmodified) fullerene suspensions. On the other hand, a modification of the C-60 core by the attachment of various functional groups results in the formation of water-soluble fullerene derivatives. Assessment of toxicity associated with C-60 preparations is of pivotal importance for their biomedical application as cytoprotective (antioxidant), cytotoxic (anticancer), or drug delivery agents. Moreover, the widespread industrial utilization of fullerenes may also have implications for human health. However, the alterations in physicochemical properties imposed by the utilization of different methods for C-60 solubilization profoundly influence toxicological effects of fullerene preparations, thus making the analysis of their potential therapeutic and environmental toxicity difficult. This review provides a comprehensive evaluation of the in vitro and in vivo toxicity of fullerenes, focusing on the comparison between pristine and derivatized C-60 preparations and the mechanisms of their toxicity to mammalian cells and tissues.",
journal = "Archives of Toxicology",
title = "Toxicity of pristine versus functionalized fullerenes: mechanisms of cell damage and the role of oxidative stress",
volume = "86",
number = "12",
pages = "1809-1827",
doi = "10.1007/s00204-012-0859-6"
}

Trpković, A., Todorović-Marković, B.,& Trajković, V. S.. (2012). Toxicity of pristine versus functionalized fullerenes: mechanisms of cell damage and the role of oxidative stress. in Archives of Toxicology, 86(12), 1809-1827.
https://doi.org/10.1007/s00204-012-0859-6

Trpković A, Todorović-Marković B, Trajković VS. Toxicity of pristine versus functionalized fullerenes: mechanisms of cell damage and the role of oxidative stress. in Archives of Toxicology. 2012;86(12):1809-1827.
doi:10.1007/s00204-012-0859-6 .

Trpković, Andreja, Todorović-Marković, Biljana, Trajković, Vladimir S., "Toxicity of pristine versus functionalized fullerenes: mechanisms of cell damage and the role of oxidative stress" in Archives of Toxicology, 86, no. 12 (2012):1809-1827,
https://doi.org/10.1007/s00204-012-0859-6 . .

TY  - JOUR
AU  - Nikolić, Dragana
AU  - Gluvić, Zoran
AU  - Akšam, Slavica
AU  - Obradović, Milan M.
AU  - Dobutović, Branislava
AU  - Soskić, Sanja S.
AU  - Sudar, Emina
AU  - Trpković, Andreja
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10327
AB  - Oksidativni stres (OxS) je skup poremećaja dinamičke ravnoteže prooksidanasa i antioksidanasa koji nastaje usled povećane produkcije slobodnih radikala (SR) ili usled smanjene aktivnosti antioksidativnog zaštitnog sistema (AOS). Bolest koja se, takođe, povezuje sa OxS je i diabetes mellitus (DM). DM karakteriše povećani nivo glukoze u cirkulaciji, kao i drugi biohemijski poremećaji koji nastaju kao posledica neadekvatne produkcije ili neadekvatnog dejstva insulina. Dijabetes tipa 1 (DMT1) je prototip autoimune bolesti sa intenzivnim OxS. Antioksidativni enzim katalaza (CAT) smanjuje produkciju vodonik-peroksida koji može biti veoma toksičan za ćelije pankreasa. Povećanje aktivnosti CAT u svim fazama DMT1 indirektno potvrđuje značaj OxS u nastanku ove bolesti. Visoko reaktivni SR, nastali uglavnom zbog hiperglikemije, izazivaju OxS što dodatno ubrzava razvoj i napredovanje DM kao i njegovih komplikacija koje su uzrokovane redukovanom aktivnošću AOS. Uprkos brojnim dokazima o štetnim posledicama OxS u DM, veliki broj kliničkih ispitivanja sa klasičnim antioksidansima, nažalost, nije pokazao efikasnost njihove primene u lečenju DM. Novi terapijski pristup, koji uključuje primenu kako standardnih tako i novih antioksidanasa, se predlaže u algoritmima lečenja DM. Važno je ukazati na značaj doze primenjenih antioksidanasa, obzirom da je dokazano da pojedinačne visoke doze mogu delovati prooksidaciono. Takođe, važna je i dozna uravnoteženost primenjenih antioksidanasa i antidijabetika, u cilju efikasnijeg lečenja obolelih od DM. U okviru ovog rada fokusirali smo se na ulogu antioksidansa u lečenju DM.
AB  - Oxidative stress (OxS) represents an imbalance in dynamic equilibrium between prooxidants and antioxidants caused by increased free radical (FR) production or decreased activity of antioxidative system (AOS). OxS is involvedin many diseases such is diabetes mellitus (DM). DM presents with elevated blood glucose level and other biochemical disorders related to the inappropriate insulin secretion or improper insulin action. DM type 1 (DMT1) is an autoimmune disease with excessive OxS. The activity of antioxidative enzyme catalase (CAT) diminishes the production of hydrogen peroxide which is highly toxic for pancreatic cells. The increased activity of catalase (CAT) found in DMT1 patients signifies the importance of OxS in the pathogenesis of this disease. The generation of highly reactive FR, induced by hyperglycaemia, triggers the development of oxidative stress. Furthermore, OxS accelerates the development of DM and its complications which are related to the decreased activity of AOS. However, the standard antioxidant drugs failed in clinical trials for DM. New antioxidant agents combined with standard drugs are now proposed in therapy for DM. It is important to acknowledge that high doses of antioxidant agents could paradoxically have prooxidant effect. In addition, it is important to establish the dosage balance between antioxidant and antidiabetic drugs. In this article, we discuss the antioxidative agents and their significance in treatment of DM.
T2  - Medicinska istraživanja
T1  - Uloga antioksidanasa u lečenju diabetes mellitus-a
T1  - The role of antioxidative treatment in diabetes mellitus
VL  - 45
IS  - 2
SP  - 4
EP  - 12
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10327
ER  - 

@article{
author = "Nikolić, Dragana and Gluvić, Zoran and Akšam, Slavica and Obradović, Milan M. and Dobutović, Branislava and Soskić, Sanja S. and Sudar, Emina and Trpković, Andreja and Isenović, Esma R.",
year = "2011",
abstract = "Oksidativni stres (OxS) je skup poremećaja dinamičke ravnoteže prooksidanasa i antioksidanasa koji nastaje usled povećane produkcije slobodnih radikala (SR) ili usled smanjene aktivnosti antioksidativnog zaštitnog sistema (AOS). Bolest koja se, takođe, povezuje sa OxS je i diabetes mellitus (DM). DM karakteriše povećani nivo glukoze u cirkulaciji, kao i drugi biohemijski poremećaji koji nastaju kao posledica neadekvatne produkcije ili neadekvatnog dejstva insulina. Dijabetes tipa 1 (DMT1) je prototip autoimune bolesti sa intenzivnim OxS. Antioksidativni enzim katalaza (CAT) smanjuje produkciju vodonik-peroksida koji može biti veoma toksičan za ćelije pankreasa. Povećanje aktivnosti CAT u svim fazama DMT1 indirektno potvrđuje značaj OxS u nastanku ove bolesti. Visoko reaktivni SR, nastali uglavnom zbog hiperglikemije, izazivaju OxS što dodatno ubrzava razvoj i napredovanje DM kao i njegovih komplikacija koje su uzrokovane redukovanom aktivnošću AOS. Uprkos brojnim dokazima o štetnim posledicama OxS u DM, veliki broj kliničkih ispitivanja sa klasičnim antioksidansima, nažalost, nije pokazao efikasnost njihove primene u lečenju DM. Novi terapijski pristup, koji uključuje primenu kako standardnih tako i novih antioksidanasa, se predlaže u algoritmima lečenja DM. Važno je ukazati na značaj doze primenjenih antioksidanasa, obzirom da je dokazano da pojedinačne visoke doze mogu delovati prooksidaciono. Takođe, važna je i dozna uravnoteženost primenjenih antioksidanasa i antidijabetika, u cilju efikasnijeg lečenja obolelih od DM. U okviru ovog rada fokusirali smo se na ulogu antioksidansa u lečenju DM., Oxidative stress (OxS) represents an imbalance in dynamic equilibrium between prooxidants and antioxidants caused by increased free radical (FR) production or decreased activity of antioxidative system (AOS). OxS is involvedin many diseases such is diabetes mellitus (DM). DM presents with elevated blood glucose level and other biochemical disorders related to the inappropriate insulin secretion or improper insulin action. DM type 1 (DMT1) is an autoimmune disease with excessive OxS. The activity of antioxidative enzyme catalase (CAT) diminishes the production of hydrogen peroxide which is highly toxic for pancreatic cells. The increased activity of catalase (CAT) found in DMT1 patients signifies the importance of OxS in the pathogenesis of this disease. The generation of highly reactive FR, induced by hyperglycaemia, triggers the development of oxidative stress. Furthermore, OxS accelerates the development of DM and its complications which are related to the decreased activity of AOS. However, the standard antioxidant drugs failed in clinical trials for DM. New antioxidant agents combined with standard drugs are now proposed in therapy for DM. It is important to acknowledge that high doses of antioxidant agents could paradoxically have prooxidant effect. In addition, it is important to establish the dosage balance between antioxidant and antidiabetic drugs. In this article, we discuss the antioxidative agents and their significance in treatment of DM.",
journal = "Medicinska istraživanja",
title = "Uloga antioksidanasa u lečenju diabetes mellitus-a, The role of antioxidative treatment in diabetes mellitus",
volume = "45",
number = "2",
pages = "4-12",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10327"
}

Nikolić, D., Gluvić, Z., Akšam, S., Obradović, M. M., Dobutović, B., Soskić, S. S., Sudar, E., Trpković, A.,& Isenović, E. R.. (2011). Uloga antioksidanasa u lečenju diabetes mellitus-a. in Medicinska istraživanja, 45(2), 4-12.
https://hdl.handle.net/21.15107/rcub_vinar_10327

Nikolić D, Gluvić Z, Akšam S, Obradović MM, Dobutović B, Soskić SS, Sudar E, Trpković A, Isenović ER. Uloga antioksidanasa u lečenju diabetes mellitus-a. in Medicinska istraživanja. 2011;45(2):4-12.
https://hdl.handle.net/21.15107/rcub_vinar_10327 .

Nikolić, Dragana, Gluvić, Zoran, Akšam, Slavica, Obradović, Milan M., Dobutović, Branislava, Soskić, Sanja S., Sudar, Emina, Trpković, Andreja, Isenović, Esma R., "Uloga antioksidanasa u lečenju diabetes mellitus-a" in Medicinska istraživanja, 45, no. 2 (2011):4-12,
https://hdl.handle.net/21.15107/rcub_vinar_10327 .

TY  - JOUR
AU  - Trpković, Andreja
AU  - Todorović-Marković, Biljana
AU  - Kleut, Duška
AU  - Misirkić, Maja
AU  - Janjetović, Kristina D.
AU  - Vucicevic, Ljubica
AU  - Pantovic, Aleksandar
AU  - Jovanović, Svetlana P.
AU  - Dramićanin, Miroslav
AU  - Marković, Zoran M.
AU  - Trajković, Vladimir S.
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4093
AB  - The present study investigated the hemolytic properties of fullerene (C-60) nanoparticles prepared by solvent exchange using tetrahydrofuran (nC(60)THF), or by mechanochemically assisted complexation with macrocyclic oligosaccharide gamma-cyclodextrin (nC(60)CDX) or the copolymer ethylene vinyl acetate-ethylene vinyl versatate (nC(60)EVA-EVV). The spectrophotometrical analysis of hemoglobin release revealed that only nC(60)THF, but not nC(60)CDX or nC(60)EVA-EVV, was able to cause lysis of human erythrocytes in a dose-and time-dependent manner. Atomic force microscopy revealed that nC(60)THF-mediated hemolysis was preceded by erythrocyte shrinkage and increase in cell surface roughness. A flow cytometric analysis confirmed a decrease in erythrocyte size and demonstrated a significant increase in reactive oxygen species production in red blood cells exposed to nC(60)THF. The nC(60)THF-triggered hemolytic activity was efficiently reduced by the antioxidants N-acetylcysteine and butylated hydroxyanisole, as well as by serum albumin, the most abundant protein in human blood plasma. These data indicate that nC(60)THF can cause serum albumin-preventable hemolysis through oxidative stress-mediated damage of the erythrocyte membrane.
T2  - Nanotechnology
T1  - Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles
VL  - 21
IS  - 37
DO  - 10.1088/0957-4484/21/37/375102
ER  - 

@article{
author = "Trpković, Andreja and Todorović-Marković, Biljana and Kleut, Duška and Misirkić, Maja and Janjetović, Kristina D. and Vucicevic, Ljubica and Pantovic, Aleksandar and Jovanović, Svetlana P. and Dramićanin, Miroslav and Marković, Zoran M. and Trajković, Vladimir S.",
year = "2010",
abstract = "The present study investigated the hemolytic properties of fullerene (C-60) nanoparticles prepared by solvent exchange using tetrahydrofuran (nC(60)THF), or by mechanochemically assisted complexation with macrocyclic oligosaccharide gamma-cyclodextrin (nC(60)CDX) or the copolymer ethylene vinyl acetate-ethylene vinyl versatate (nC(60)EVA-EVV). The spectrophotometrical analysis of hemoglobin release revealed that only nC(60)THF, but not nC(60)CDX or nC(60)EVA-EVV, was able to cause lysis of human erythrocytes in a dose-and time-dependent manner. Atomic force microscopy revealed that nC(60)THF-mediated hemolysis was preceded by erythrocyte shrinkage and increase in cell surface roughness. A flow cytometric analysis confirmed a decrease in erythrocyte size and demonstrated a significant increase in reactive oxygen species production in red blood cells exposed to nC(60)THF. The nC(60)THF-triggered hemolytic activity was efficiently reduced by the antioxidants N-acetylcysteine and butylated hydroxyanisole, as well as by serum albumin, the most abundant protein in human blood plasma. These data indicate that nC(60)THF can cause serum albumin-preventable hemolysis through oxidative stress-mediated damage of the erythrocyte membrane.",
journal = "Nanotechnology",
title = "Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles",
volume = "21",
number = "37",
doi = "10.1088/0957-4484/21/37/375102"
}

Trpković, A., Todorović-Marković, B., Kleut, D., Misirkić, M., Janjetović, K. D., Vucicevic, L., Pantovic, A., Jovanović, S. P., Dramićanin, M., Marković, Z. M.,& Trajković, V. S.. (2010). Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles. in Nanotechnology, 21(37).
https://doi.org/10.1088/0957-4484/21/37/375102

Trpković A, Todorović-Marković B, Kleut D, Misirkić M, Janjetović KD, Vucicevic L, Pantovic A, Jovanović SP, Dramićanin M, Marković ZM, Trajković VS. Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles. in Nanotechnology. 2010;21(37).
doi:10.1088/0957-4484/21/37/375102 .

Trpković, Andreja, Todorović-Marković, Biljana, Kleut, Duška, Misirkić, Maja, Janjetović, Kristina D., Vucicevic, Ljubica, Pantovic, Aleksandar, Jovanović, Svetlana P., Dramićanin, Miroslav, Marković, Zoran M., Trajković, Vladimir S., "Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles" in Nanotechnology, 21, no. 37 (2010),
https://doi.org/10.1088/0957-4484/21/37/375102 . .

TY  - JOUR
AU  - Trpković, Andreja
AU  - Stokić, Edita
AU  - Radak, Đorđe J.
AU  - Gluvić, Zoran
AU  - Haidara, Mohamed A.
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4208
AB  - The role of hepatitis C virus (HCV) infection in the development of vascular disease is controversial. Insulin resistance (IR) is a recognized risk factor for cardiovascular disease (CVD) and is associated with chronic hepatitis C (CHC). Thus, IR may promote atherosclerosis and vascular disease in CHC patients. HCV-associated IR may also cause hepatic steatosis and resistance to antiviral treatment. In addition, HCV may contribute a direct, proatherogenetic action on the vascular wall. This review considers the impact of IR on interferon-based therapy of HCV infection and the role of insulin-sensitizing agents on the response to antiviral treatment and prevention of IR complications, including CVD.
T2  - Current Pharmaceutical Design
T1  - Chronic Hepatitis C, Insulin Resistance and Vascular Disease
VL  - 16
IS  - 34
SP  - 3823
EP  - 3829
DO  - 10.2174/138161210794455067
ER  - 

@article{
author = "Trpković, Andreja and Stokić, Edita and Radak, Đorđe J. and Gluvić, Zoran and Haidara, Mohamed A. and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2010",
abstract = "The role of hepatitis C virus (HCV) infection in the development of vascular disease is controversial. Insulin resistance (IR) is a recognized risk factor for cardiovascular disease (CVD) and is associated with chronic hepatitis C (CHC). Thus, IR may promote atherosclerosis and vascular disease in CHC patients. HCV-associated IR may also cause hepatic steatosis and resistance to antiviral treatment. In addition, HCV may contribute a direct, proatherogenetic action on the vascular wall. This review considers the impact of IR on interferon-based therapy of HCV infection and the role of insulin-sensitizing agents on the response to antiviral treatment and prevention of IR complications, including CVD.",
journal = "Current Pharmaceutical Design",
title = "Chronic Hepatitis C, Insulin Resistance and Vascular Disease",
volume = "16",
number = "34",
pages = "3823-3829",
doi = "10.2174/138161210794455067"
}

Trpković, A., Stokić, E., Radak, Đ. J., Gluvić, Z., Haidara, M. A., Mikhailidis, D. P.,& Isenović, E. R.. (2010). Chronic Hepatitis C, Insulin Resistance and Vascular Disease. in Current Pharmaceutical Design, 16(34), 3823-3829.
https://doi.org/10.2174/138161210794455067

Trpković A, Stokić E, Radak ĐJ, Gluvić Z, Haidara MA, Mikhailidis DP, Isenović ER. Chronic Hepatitis C, Insulin Resistance and Vascular Disease. in Current Pharmaceutical Design. 2010;16(34):3823-3829.
doi:10.2174/138161210794455067 .

Trpković, Andreja, Stokić, Edita, Radak, Đorđe J., Gluvić, Zoran, Haidara, Mohamed A., Mikhailidis, Dimitri P., Isenović, Esma R., "Chronic Hepatitis C, Insulin Resistance and Vascular Disease" in Current Pharmaceutical Design, 16, no. 34 (2010):3823-3829,
https://doi.org/10.2174/138161210794455067 . .

TY  - JOUR
AU  - Gluvić, Zoran
AU  - Tica, Jelena S.
AU  - Vujović, Marina V.
AU  - Rašić-Milutinović, Zorica R.
AU  - Popović-Radinović, Vesna
AU  - Lačković, Milena M.
AU  - Trpković, Andreja T.
AU  - Isenović, Esma R.
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10328
AB  - Subklinički hipotiroidizam je asimptomatska ili simptomatska tiroidna disfunkcija, koja se karakteriše umerenim porastom nivoa TSH i normalnim nivoima perifernih tiroidnih hormona. Često se otkriva uzgredno. Etiologija subkliničkog hipotiroidizma je identična etiologiji kliničkog hipotiroidizma. Dijagnostikuje se laboratorijski, određivanjem nivoa TSH i perifernih tirodnih frakcija. S'obzirom da je od kliničkog značaja samo perzistentni subklinički hipotiroidizam, za definitivnu potvrdu je neophodno učiniti hormonsku reevaluaciju 6-12 meseci nakon incijalne. Značaj subkliničkog hipotiroidizma je prevashodno u postojanju određenih propratnih pojava, koje mogu značajno uticati na kvalitet života bolesnika (dislipidemija, kardiovaskularni i neurokognitivni poremećaji, infertilitet, poremećaj intrauterinog razvoja ploda). Upravo stoga, lečenje subkliničkog hipotiroidizma malim dozama levotiroksina treba sprovesti u slučajevima gde je korist od supstitucije daleko veća od njenih potencijalnih rizika. Ovaj revijski rad je pokušaj argumentovanog razmatranja kliničkih i terapijskih aspekata subkliničkog hipotiroidizma iz literature i našeg kliničkog iskustva.
AB  - Subclinical hypothyroidism is asymptomatic or symptomatic thyroid dysfunction, presented as slightly elevated TSH level and reference range values of peripheral thyroid hormons. Its etiology is the same as the etiology of clinical hypothyroidism. By measurement of TSH serum level as well the levels of peripheral free thyroid hormone fractions, it is easy, but more frequently incidental, diagnosed. Because of clinical significance is just persistent subclinical hypothyroidism, obliged hormonal confirmation would be done 6-12 months after initial measurement. The importance of subclinical hypothyroidism lay in the co-existence of some accompanying phenomenons, which can significantly influence on the patients life quality (lipid disorders, cardiovascular and neurocognitive dysfunctions, infertility, inadequate fetal growth and deveolpment). For such reasons, it is necessary to substitute subclinical hypothyroidism with small doses of levothyroxine, where we can expect more benefit than the risk of therapy. This review article is an attempt to unite present important clinical and therapeutical aspects of subclinical hypothyroidism from reviews and our experience.
T2  - Materia medica
T1  - Subklinički hipotiroidizam
T1  - Subclinical hypothyroidism
VL  - 26
IS  - 3
SP  - 95
EP  - 100
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10328
ER  - 

@article{
author = "Gluvić, Zoran and Tica, Jelena S. and Vujović, Marina V. and Rašić-Milutinović, Zorica R. and Popović-Radinović, Vesna and Lačković, Milena M. and Trpković, Andreja T. and Isenović, Esma R.",
year = "2010",
abstract = "Subklinički hipotiroidizam je asimptomatska ili simptomatska tiroidna disfunkcija, koja se karakteriše umerenim porastom nivoa TSH i normalnim nivoima perifernih tiroidnih hormona. Često se otkriva uzgredno. Etiologija subkliničkog hipotiroidizma je identična etiologiji kliničkog hipotiroidizma. Dijagnostikuje se laboratorijski, određivanjem nivoa TSH i perifernih tirodnih frakcija. S'obzirom da je od kliničkog značaja samo perzistentni subklinički hipotiroidizam, za definitivnu potvrdu je neophodno učiniti hormonsku reevaluaciju 6-12 meseci nakon incijalne. Značaj subkliničkog hipotiroidizma je prevashodno u postojanju određenih propratnih pojava, koje mogu značajno uticati na kvalitet života bolesnika (dislipidemija, kardiovaskularni i neurokognitivni poremećaji, infertilitet, poremećaj intrauterinog razvoja ploda). Upravo stoga, lečenje subkliničkog hipotiroidizma malim dozama levotiroksina treba sprovesti u slučajevima gde je korist od supstitucije daleko veća od njenih potencijalnih rizika. Ovaj revijski rad je pokušaj argumentovanog razmatranja kliničkih i terapijskih aspekata subkliničkog hipotiroidizma iz literature i našeg kliničkog iskustva., Subclinical hypothyroidism is asymptomatic or symptomatic thyroid dysfunction, presented as slightly elevated TSH level and reference range values of peripheral thyroid hormons. Its etiology is the same as the etiology of clinical hypothyroidism. By measurement of TSH serum level as well the levels of peripheral free thyroid hormone fractions, it is easy, but more frequently incidental, diagnosed. Because of clinical significance is just persistent subclinical hypothyroidism, obliged hormonal confirmation would be done 6-12 months after initial measurement. The importance of subclinical hypothyroidism lay in the co-existence of some accompanying phenomenons, which can significantly influence on the patients life quality (lipid disorders, cardiovascular and neurocognitive dysfunctions, infertility, inadequate fetal growth and deveolpment). For such reasons, it is necessary to substitute subclinical hypothyroidism with small doses of levothyroxine, where we can expect more benefit than the risk of therapy. This review article is an attempt to unite present important clinical and therapeutical aspects of subclinical hypothyroidism from reviews and our experience.",
journal = "Materia medica",
title = "Subklinički hipotiroidizam, Subclinical hypothyroidism",
volume = "26",
number = "3",
pages = "95-100",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10328"
}

Gluvić, Z., Tica, J. S., Vujović, M. V., Rašić-Milutinović, Z. R., Popović-Radinović, V., Lačković, M. M., Trpković, A. T.,& Isenović, E. R.. (2010). Subklinički hipotiroidizam. in Materia medica, 26(3), 95-100.
https://hdl.handle.net/21.15107/rcub_vinar_10328

Gluvić Z, Tica JS, Vujović MV, Rašić-Milutinović ZR, Popović-Radinović V, Lačković MM, Trpković AT, Isenović ER. Subklinički hipotiroidizam. in Materia medica. 2010;26(3):95-100.
https://hdl.handle.net/21.15107/rcub_vinar_10328 .

Gluvić, Zoran, Tica, Jelena S., Vujović, Marina V., Rašić-Milutinović, Zorica R., Popović-Radinović, Vesna, Lačković, Milena M., Trpković, Andreja T., Isenović, Esma R., "Subklinički hipotiroidizam" in Materia medica, 26, no. 3 (2010):95-100,
https://hdl.handle.net/21.15107/rcub_vinar_10328 .

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Soskić, Sanja S.
AU  - Trpković, Andreja
AU  - Dobutović, Branislava
AU  - Popović, Milan
AU  - Gluvić, Zoran
AU  - Putniković, Biljana
AU  - Marche, Pierre
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4209
AB  - Vascular smooth muscle cells (VSMC) respond to arterial wall injury by intimal proliferation and play a key role in atherogenesis by proliferating and migrating excessively in response to repeated injury, such as hypertension and atherosclerosis. In contrast, fully differentiated, quiescent VSMC allow arterial vasodilatation and vasoconstriction. Exaggerated and uncontrolled VSMC proliferation appears therefore to be a common feature of both atherosclerosis and hypertension. Signal transduction pathways in eukaryotic cells integrate diverse extracellular signals, and regulate complex biological responses such as growth, differentiation and death. One group of proline-directed Ser/Thr protein kinases, the mitogen-activated protein kinases (MAPKs), plays a central role in these signalling pathways. Much attention has focused in recent years on subfamilies of MAPKs, the extracellular signal regulated kinases (ERKs). Here we overview the work on ERKs 1 to 2, emphasising when possible their biological activities in VSMC proliferation. It is clear from numerosus studies including our own, that ERK1/ERK2 pathway has an imoprtant role in VSMC proliferation induced by insulin (INS) and thrombin. Despite the physiological and pathophysiological importance of INS and thrombin, possible signal transduction pathways involved in INS and thrombin regulation of VSMCs proliferation remains poorly understood. Thus, this review examines recent findings in signalling mechanisms involved in INS and thrombin-triggered VSMCs proliferation with particular emphasis on ERK1/2 signalling pathways. Future investigations should now focus on the mechanisms of MAPK activation which might therefore represent a new mechanism involved in the antiproliferative effect revealed in this review.
T2  - Current Pharmaceutical Design
T1  - Insulin, Thrombin, ERK1/2 Kinase and Vascular Smooth Muscle Cells Proliferation
VL  - 16
IS  - 35
SP  - 3895
EP  - 3902
DO  - 10.2174/138161210794454987
ER  - 

@article{
author = "Isenović, Esma R. and Soskić, Sanja S. and Trpković, Andreja and Dobutović, Branislava and Popović, Milan and Gluvić, Zoran and Putniković, Biljana and Marche, Pierre",
year = "2010",
abstract = "Vascular smooth muscle cells (VSMC) respond to arterial wall injury by intimal proliferation and play a key role in atherogenesis by proliferating and migrating excessively in response to repeated injury, such as hypertension and atherosclerosis. In contrast, fully differentiated, quiescent VSMC allow arterial vasodilatation and vasoconstriction. Exaggerated and uncontrolled VSMC proliferation appears therefore to be a common feature of both atherosclerosis and hypertension. Signal transduction pathways in eukaryotic cells integrate diverse extracellular signals, and regulate complex biological responses such as growth, differentiation and death. One group of proline-directed Ser/Thr protein kinases, the mitogen-activated protein kinases (MAPKs), plays a central role in these signalling pathways. Much attention has focused in recent years on subfamilies of MAPKs, the extracellular signal regulated kinases (ERKs). Here we overview the work on ERKs 1 to 2, emphasising when possible their biological activities in VSMC proliferation. It is clear from numerosus studies including our own, that ERK1/ERK2 pathway has an imoprtant role in VSMC proliferation induced by insulin (INS) and thrombin. Despite the physiological and pathophysiological importance of INS and thrombin, possible signal transduction pathways involved in INS and thrombin regulation of VSMCs proliferation remains poorly understood. Thus, this review examines recent findings in signalling mechanisms involved in INS and thrombin-triggered VSMCs proliferation with particular emphasis on ERK1/2 signalling pathways. Future investigations should now focus on the mechanisms of MAPK activation which might therefore represent a new mechanism involved in the antiproliferative effect revealed in this review.",
journal = "Current Pharmaceutical Design",
title = "Insulin, Thrombin, ERK1/2 Kinase and Vascular Smooth Muscle Cells Proliferation",
volume = "16",
number = "35",
pages = "3895-3902",
doi = "10.2174/138161210794454987"
}

Isenović, E. R., Soskić, S. S., Trpković, A., Dobutović, B., Popović, M., Gluvić, Z., Putniković, B.,& Marche, P.. (2010). Insulin, Thrombin, ERK1/2 Kinase and Vascular Smooth Muscle Cells Proliferation. in Current Pharmaceutical Design, 16(35), 3895-3902.
https://doi.org/10.2174/138161210794454987

Isenović ER, Soskić SS, Trpković A, Dobutović B, Popović M, Gluvić Z, Putniković B, Marche P. Insulin, Thrombin, ERK1/2 Kinase and Vascular Smooth Muscle Cells Proliferation. in Current Pharmaceutical Design. 2010;16(35):3895-3902.
doi:10.2174/138161210794454987 .

Isenović, Esma R., Soskić, Sanja S., Trpković, Andreja, Dobutović, Branislava, Popović, Milan, Gluvić, Zoran, Putniković, Biljana, Marche, Pierre, "Insulin, Thrombin, ERK1/2 Kinase and Vascular Smooth Muscle Cells Proliferation" in Current Pharmaceutical Design, 16, no. 35 (2010):3895-3902,
https://doi.org/10.2174/138161210794454987 . .

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Kedees, Mamdouh H.
AU  - Haidara, Mohamed A.
AU  - Trpković, Andreja
AU  - Mikhailidis, Dimitri P.
AU  - Marche, Pierre
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3984
AB  - It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42- and 44-kDa isoforms (ERK1/2)participate in the cellular mitogenic machinery triggered by several VSMCs activators, including insulin (INS) and thrombin (Thr). However, understanding of the intracellular signal transduction pathways involved is incomplete. This review considers the recent findings in INS and Thr signaling mechanisms that modulate the proliferation of VSMCs with particular emphasis on the ERK1/2 signaling pathway, an important mediator of VSMCs hypertrophy and vascular disease. Moreover, because the ERK1/2 pathway have been acknowledged as an important mediator of VSMCs hypertrophy, ERK1/2 is identified as a key target for novel therapeutic interventions to minimize irreversible tissue damage associated with hypertension and atherosclerosis.
T2  - Angiology
T1  - Involvement of ERK1/2 Kinase in Insulin- and Thrombin-Stimulated Vascular Smooth Muscle Cell Proliferation
VL  - 61
IS  - 4
SP  - 357
EP  - 364
DO  - 10.1177/0003319709358693
ER  - 

@article{
author = "Isenović, Esma R. and Kedees, Mamdouh H. and Haidara, Mohamed A. and Trpković, Andreja and Mikhailidis, Dimitri P. and Marche, Pierre",
year = "2010",
abstract = "It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42- and 44-kDa isoforms (ERK1/2)participate in the cellular mitogenic machinery triggered by several VSMCs activators, including insulin (INS) and thrombin (Thr). However, understanding of the intracellular signal transduction pathways involved is incomplete. This review considers the recent findings in INS and Thr signaling mechanisms that modulate the proliferation of VSMCs with particular emphasis on the ERK1/2 signaling pathway, an important mediator of VSMCs hypertrophy and vascular disease. Moreover, because the ERK1/2 pathway have been acknowledged as an important mediator of VSMCs hypertrophy, ERK1/2 is identified as a key target for novel therapeutic interventions to minimize irreversible tissue damage associated with hypertension and atherosclerosis.",
journal = "Angiology",
title = "Involvement of ERK1/2 Kinase in Insulin- and Thrombin-Stimulated Vascular Smooth Muscle Cell Proliferation",
volume = "61",
number = "4",
pages = "357-364",
doi = "10.1177/0003319709358693"
}

Isenović, E. R., Kedees, M. H., Haidara, M. A., Trpković, A., Mikhailidis, D. P.,& Marche, P.. (2010). Involvement of ERK1/2 Kinase in Insulin- and Thrombin-Stimulated Vascular Smooth Muscle Cell Proliferation. in Angiology, 61(4), 357-364.
https://doi.org/10.1177/0003319709358693

Isenović ER, Kedees MH, Haidara MA, Trpković A, Mikhailidis DP, Marche P. Involvement of ERK1/2 Kinase in Insulin- and Thrombin-Stimulated Vascular Smooth Muscle Cell Proliferation. in Angiology. 2010;61(4):357-364.
doi:10.1177/0003319709358693 .

Isenović, Esma R., Kedees, Mamdouh H., Haidara, Mohamed A., Trpković, Andreja, Mikhailidis, Dimitri P., Marche, Pierre, "Involvement of ERK1/2 Kinase in Insulin- and Thrombin-Stimulated Vascular Smooth Muscle Cell Proliferation" in Angiology, 61, no. 4 (2010):357-364,
https://doi.org/10.1177/0003319709358693 . .

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Kedees, Mamdouh H.
AU  - Tepavčević, Snežana
AU  - Milosavljević, Tijana
AU  - Korićanac, Goran
AU  - Trpković, Andreja
AU  - Marche, Pierre
PY  - 2009
UR  - http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1871-529X&volume=9&issue=3&spage=172
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7802
AB  - Vascular smooth muscle cells (VSMCs) respond to arterial wall injury by intimal proliferation and play a key role in atherogenesis by proliferating and migrating excessively in response to repeated injury, such as hypertension and atherosclerosis. In contrast, fully differentiated, quiescent VSMCs allow arterial vasodilatation and vasoconstriction. Exaggerated and uncontrolled VSMCs proliferation appears therefore to be a common feature of both atherosclerosis and hypertension. Phosphorylation/dephosphorylation reactions of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs), phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) as well as Akt and cytosolic phospholipase 2 (cPLA 2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including insulin (INS). The ability of INS to significantly increase VSMCs proliferation has been demonstrated in several systems, but understanding of the intracellular signal transduction pathways involved is incomplete. Signal transduction pathways involved in regulation of the VSMCs proliferation by INS remains poorly understood. Thus, this review examines recent findings in signaling mechanisms employed by INS in modulating the regulation of proliferation of VSMCs with particular emphasis on PI3K/Akt, cPLA2 and ERK1/2 signaling pathways that have been identified as important mediators of VSMCs hypertrophy and vascular diseases. These findings are critical for understanding the role of INS in vascular biology and hyperinsulinemia.
T2  - Cardiovascular and Hematological Disorders-Drug Targets
T1  - Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation
VL  - 9
IS  - 3
SP  - 172
EP  - 180
DO  - 10.2174/187152909789007034
ER  - 

@article{
author = "Isenović, Esma R. and Kedees, Mamdouh H. and Tepavčević, Snežana and Milosavljević, Tijana and Korićanac, Goran and Trpković, Andreja and Marche, Pierre",
year = "2009",
abstract = "Vascular smooth muscle cells (VSMCs) respond to arterial wall injury by intimal proliferation and play a key role in atherogenesis by proliferating and migrating excessively in response to repeated injury, such as hypertension and atherosclerosis. In contrast, fully differentiated, quiescent VSMCs allow arterial vasodilatation and vasoconstriction. Exaggerated and uncontrolled VSMCs proliferation appears therefore to be a common feature of both atherosclerosis and hypertension. Phosphorylation/dephosphorylation reactions of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs), phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) as well as Akt and cytosolic phospholipase 2 (cPLA 2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including insulin (INS). The ability of INS to significantly increase VSMCs proliferation has been demonstrated in several systems, but understanding of the intracellular signal transduction pathways involved is incomplete. Signal transduction pathways involved in regulation of the VSMCs proliferation by INS remains poorly understood. Thus, this review examines recent findings in signaling mechanisms employed by INS in modulating the regulation of proliferation of VSMCs with particular emphasis on PI3K/Akt, cPLA2 and ERK1/2 signaling pathways that have been identified as important mediators of VSMCs hypertrophy and vascular diseases. These findings are critical for understanding the role of INS in vascular biology and hyperinsulinemia.",
journal = "Cardiovascular and Hematological Disorders-Drug Targets",
title = "Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation",
volume = "9",
number = "3",
pages = "172-180",
doi = "10.2174/187152909789007034"
}

Isenović, E. R., Kedees, M. H., Tepavčević, S., Milosavljević, T., Korićanac, G., Trpković, A.,& Marche, P.. (2009). Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation. in Cardiovascular and Hematological Disorders-Drug Targets, 9(3), 172-180.
https://doi.org/10.2174/187152909789007034

Isenović ER, Kedees MH, Tepavčević S, Milosavljević T, Korićanac G, Trpković A, Marche P. Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation. in Cardiovascular and Hematological Disorders-Drug Targets. 2009;9(3):172-180.
doi:10.2174/187152909789007034 .

Isenović, Esma R., Kedees, Mamdouh H., Tepavčević, Snežana, Milosavljević, Tijana, Korićanac, Goran, Trpković, Andreja, Marche, Pierre, "Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation" in Cardiovascular and Hematological Disorders-Drug Targets, 9, no. 3 (2009):172-180,
https://doi.org/10.2174/187152909789007034 . .

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Kedees, Mamdouh H.
AU  - Tepavčević, Snežana
AU  - Milosavljević, Tijana
AU  - Korićanac, Goran
AU  - Trpković, Andreja
AU  - Marche, Pierre
PY  - 2009
UR  - http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1871-529X&volume=9&issue=3&spage=172
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7832
AB  - Vascular smooth muscle cells (VSMCs) respond to arterial wall injury by intimal proliferation and play a key role in atherogenesis by proliferating and migrating excessively in response to repeated injury, such as hypertension and atherosclerosis. In contrast, fully differentiated, quiescent VSMCs allow arterial vasodilatation and vasoconstriction. Exaggerated and uncontrolled VSMCs proliferation appears therefore to be a common feature of both atherosclerosis and hypertension. Phosphorylation/dephosphorylation reactions of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs), phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) as well as Akt and cytosolic phospholipase 2 (cPLA 2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including insulin (INS). The ability of INS to significantly increase VSMCs proliferation has been demonstrated in several systems, but understanding of the intracellular signal transduction pathways involved is incomplete. Signal transduction pathways involved in regulation of the VSMCs proliferation by INS remains poorly understood. Thus, this review examines recent findings in signaling mechanisms employed by INS in modulating the regulation of proliferation of VSMCs with particular emphasis on PI3K/Akt, cPLA2 and ERK1/2 signaling pathways that have been identified as important mediators of VSMCs hypertrophy and vascular diseases. These findings are critical for understanding the role of INS in vascular biology and hyperinsulinemia.
T2  - Cardiovascular and Hematological Disorders-Drug Targets
T1  - Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation
VL  - 9
IS  - 3
SP  - 172
EP  - 180
DO  - 10.2174/187152909789007034
ER  - 

@article{
author = "Isenović, Esma R. and Kedees, Mamdouh H. and Tepavčević, Snežana and Milosavljević, Tijana and Korićanac, Goran and Trpković, Andreja and Marche, Pierre",
year = "2009",
abstract = "Vascular smooth muscle cells (VSMCs) respond to arterial wall injury by intimal proliferation and play a key role in atherogenesis by proliferating and migrating excessively in response to repeated injury, such as hypertension and atherosclerosis. In contrast, fully differentiated, quiescent VSMCs allow arterial vasodilatation and vasoconstriction. Exaggerated and uncontrolled VSMCs proliferation appears therefore to be a common feature of both atherosclerosis and hypertension. Phosphorylation/dephosphorylation reactions of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs), phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) as well as Akt and cytosolic phospholipase 2 (cPLA 2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including insulin (INS). The ability of INS to significantly increase VSMCs proliferation has been demonstrated in several systems, but understanding of the intracellular signal transduction pathways involved is incomplete. Signal transduction pathways involved in regulation of the VSMCs proliferation by INS remains poorly understood. Thus, this review examines recent findings in signaling mechanisms employed by INS in modulating the regulation of proliferation of VSMCs with particular emphasis on PI3K/Akt, cPLA2 and ERK1/2 signaling pathways that have been identified as important mediators of VSMCs hypertrophy and vascular diseases. These findings are critical for understanding the role of INS in vascular biology and hyperinsulinemia.",
journal = "Cardiovascular and Hematological Disorders-Drug Targets",
title = "Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation",
volume = "9",
number = "3",
pages = "172-180",
doi = "10.2174/187152909789007034"
}

Isenović, E. R., Kedees, M. H., Tepavčević, S., Milosavljević, T., Korićanac, G., Trpković, A.,& Marche, P.. (2009). Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation. in Cardiovascular and Hematological Disorders-Drug Targets, 9(3), 172-180.
https://doi.org/10.2174/187152909789007034

Isenović ER, Kedees MH, Tepavčević S, Milosavljević T, Korićanac G, Trpković A, Marche P. Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation. in Cardiovascular and Hematological Disorders-Drug Targets. 2009;9(3):172-180.
doi:10.2174/187152909789007034 .

Isenović, Esma R., Kedees, Mamdouh H., Tepavčević, Snežana, Milosavljević, Tijana, Korićanac, Goran, Trpković, Andreja, Marche, Pierre, "Role of PI3K/AKT, cPLA2 and ERK1/2 Signaling Pathways in Insulin Regulation of Vascular Smooth Muscle Cells Proliferation" in Cardiovascular and Hematological Disorders-Drug Targets, 9, no. 3 (2009):172-180,
https://doi.org/10.2174/187152909789007034 . .

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Fretaud, Maxence
AU  - Dobutović, Branislava
AU  - Sudar, Emina
AU  - Smiljanić, Katarina
AU  - Zarić, Božidarka
AU  - Trpković, Andreja
AU  - Marche, Pierre
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3644
AB  - Insulin (INS) via INS receptor acts as a mitogen in vascular smooth muscle cells (VSMCs) through stimulation of multiple signaling mechanisms, including p42/44 mitogen-activated protein kinase (ERK1/2) and phosphatidyl inositol-3 kinase (PI3K). In addition, cytosolic phospholipase 2 (cPLA(2)) is linked to VSMCs proliferation. However, the upstream mechanisms responsible for activation of cPLA(2) are not well defined. Therefore, this investigation used primary cultured rat VSMCs to examine the role of PI3K and ERK1/2 in the INS-dependent phosphorylation of cPLA(2) and proliferation induced by INS. Exposure of VSMCs to INS (100 nM) for 10 min increased the phosphorylation of cPLA(2) by 1.5-fold (p LT 0.01), which was blocked by the cPLA(2) inhibitor MAFP (10 mu M; 15 min). Similarly, the PI3K inhibitor LY294002 (10 mu M; 15 min) and ERK1/2 inhibitor PD98059 (20 mu M; 15 min) abolished the INS-mediated increase in cPLA(2) phosphorylation by 59% (p LT 0.001), and by 75% (p LT 0.001), respectively. Further, inhibition of cPLA2 with cPLA2 inhibitor MAFP abolished the INS-stimulated ERK1/2 phosphorylation by 65% (p LT 0.01). Incubation of rat VSMCs with INS resulted in an increase of VSMCs proliferation by 85% (p LT 0.001). The effect of INS on VSMCs proliferation was significantly (p LT 0.01) reduced by pretreatment with MAFP. Thus, we hypothesized that INS stimulates VSMCs proliferation via a mechanism involving the PI3K-dependent activation of cPLA(2) and release of arachidonic acid (AA), which activates ERK1/2 and further amplifies cPLA(2) activity. (C) 2009 International Federation for Cell Biology. Published by Elsevier Ltd. All rights reserved.
T2  - Cell Biology International
T1  - A novel hypothesis regarding the possible involvement of cytosolic phospholipase 2 in insulin-stimulated proliferation of vascular smooth muscle cells
VL  - 33
IS  - 3
SP  - 386
EP  - 392
DO  - 10.1016/j.cellbi.2009.01.010
ER  - 

@article{
author = "Isenović, Esma R. and Fretaud, Maxence and Dobutović, Branislava and Sudar, Emina and Smiljanić, Katarina and Zarić, Božidarka and Trpković, Andreja and Marche, Pierre",
year = "2009",
abstract = "Insulin (INS) via INS receptor acts as a mitogen in vascular smooth muscle cells (VSMCs) through stimulation of multiple signaling mechanisms, including p42/44 mitogen-activated protein kinase (ERK1/2) and phosphatidyl inositol-3 kinase (PI3K). In addition, cytosolic phospholipase 2 (cPLA(2)) is linked to VSMCs proliferation. However, the upstream mechanisms responsible for activation of cPLA(2) are not well defined. Therefore, this investigation used primary cultured rat VSMCs to examine the role of PI3K and ERK1/2 in the INS-dependent phosphorylation of cPLA(2) and proliferation induced by INS. Exposure of VSMCs to INS (100 nM) for 10 min increased the phosphorylation of cPLA(2) by 1.5-fold (p LT 0.01), which was blocked by the cPLA(2) inhibitor MAFP (10 mu M; 15 min). Similarly, the PI3K inhibitor LY294002 (10 mu M; 15 min) and ERK1/2 inhibitor PD98059 (20 mu M; 15 min) abolished the INS-mediated increase in cPLA(2) phosphorylation by 59% (p LT 0.001), and by 75% (p LT 0.001), respectively. Further, inhibition of cPLA2 with cPLA2 inhibitor MAFP abolished the INS-stimulated ERK1/2 phosphorylation by 65% (p LT 0.01). Incubation of rat VSMCs with INS resulted in an increase of VSMCs proliferation by 85% (p LT 0.001). The effect of INS on VSMCs proliferation was significantly (p LT 0.01) reduced by pretreatment with MAFP. Thus, we hypothesized that INS stimulates VSMCs proliferation via a mechanism involving the PI3K-dependent activation of cPLA(2) and release of arachidonic acid (AA), which activates ERK1/2 and further amplifies cPLA(2) activity. (C) 2009 International Federation for Cell Biology. Published by Elsevier Ltd. All rights reserved.",
journal = "Cell Biology International",
title = "A novel hypothesis regarding the possible involvement of cytosolic phospholipase 2 in insulin-stimulated proliferation of vascular smooth muscle cells",
volume = "33",
number = "3",
pages = "386-392",
doi = "10.1016/j.cellbi.2009.01.010"
}

Isenović, E. R., Fretaud, M., Dobutović, B., Sudar, E., Smiljanić, K., Zarić, B., Trpković, A.,& Marche, P.. (2009). A novel hypothesis regarding the possible involvement of cytosolic phospholipase 2 in insulin-stimulated proliferation of vascular smooth muscle cells. in Cell Biology International, 33(3), 386-392.
https://doi.org/10.1016/j.cellbi.2009.01.010

Isenović ER, Fretaud M, Dobutović B, Sudar E, Smiljanić K, Zarić B, Trpković A, Marche P. A novel hypothesis regarding the possible involvement of cytosolic phospholipase 2 in insulin-stimulated proliferation of vascular smooth muscle cells. in Cell Biology International. 2009;33(3):386-392.
doi:10.1016/j.cellbi.2009.01.010 .

Isenović, Esma R., Fretaud, Maxence, Dobutović, Branislava, Sudar, Emina, Smiljanić, Katarina, Zarić, Božidarka, Trpković, Andreja, Marche, Pierre, "A novel hypothesis regarding the possible involvement of cytosolic phospholipase 2 in insulin-stimulated proliferation of vascular smooth muscle cells" in Cell Biology International, 33, no. 3 (2009):386-392,
https://doi.org/10.1016/j.cellbi.2009.01.010 . .

TY  - JOUR
AU  - Dobutović, Branislava
AU  - Trpković, Andreja
AU  - Putniković, Biljana
AU  - Gluvić, Zoran
AU  - Isenović, Esma R.
PY  - 2008
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10330
AB  - Previous studies have reported increased myocardial inducible nitric oxide synthase (iNOs) expression and activity in chronic heart failure (ChF). Nitric oxide (NO) is a free radical which reacts with various molecules to cause multiple biological effects. Carvedilol is a α1-, β1-, and β2-adrenergic antagonist, used in therapy of hypertension and ChF. recently, it has been shown that carvedilol has an effect as NO quenching agent. Carvedilol presents several other mechanisms of action that converge to improve the symptomatology of hypertension and CHF. In addition to the adrenergic antagonism, carvedilol is also an antioxidant and endothelin suppressor. The molecular mechanism for the NO quenching potency of carvedilol remains to be determined. In cardiac cells the major pathway responsible for the regulation of iNOS activity/expression involves the activation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt). Thus, in our current ongoing and future studies, we will test the hypothesis that in disease states such as CHF where the PI3K/Akt pathway is interrupted, the regulation of iNOS activity/expression will be abolished. as a corollary of this primary hypothesis, we postulate that in CHF carvedilol stimulates cardiovascular iNOS via a mechanism involving activation of PI3K/akt cascade and further amplifies iNOS activity/expression. Moreover, since the PI3K/akt pathway have been acknowledged as a critically important mediator of cardiac iNOS regulation, PI3K/akt are identified as one of key targets for novel therapeutic interventions to minimize irreversible tissue damage associated with CHF and hypertension. A safer technology to regulate in vivo synthesis of PI3K/akt by generic manipulation would be a welcome work.
AB  - Azot oksid (NO) je slobodni radikal čije reakcije dovode do različitih bioloških dejstava. Karvedilol je antagonist α1-, β1-,i β2 adrenergičkih receptora koji se koristi u terapiji hipertenzije i nedavno je pokazano da hemijski reaguje sa NO. Pored adrenergičke blokade karvedilol doprinosi poboljšanju hipertenzije i HSI drugim mehanizmima. Takođe, pokazano je da karvedilol ima ulogu antioksidansa i ulogu u supresiji endotelina. Precizan mehanizam interakcije karvedilola i NO do sada nije u potpunosti razjašnjen. aktivnost/ekspresija inducibilne azot oksid sintetaze (iNOS) u kardiomiocitima dominantno je regulisana aktivacijom fosfatidilinozitol 3-kinaze (PI3K) i protein kinaze B (akt). U našim tekućim i planiranim istraživanjima, polazimo od hipoteze da je u HSI poremećen PI3K/akt signalni put, a time konsekventno i smanjena aktivnost/ekspresija iNOS-a. Takođe, naša hipoteza se bazira na pretpostavci da karvedilol u HSI stimuliše iNOS u kardiovaskularnom sistemu preko aktivacije PI3K/Akt kaskade. U zaključku, regulacija PI3K/Akt signalnog puta ima veoma bitnu ulogu u regulaciji iNOS-a u stanjima HSI. S obzirom da PI3K/Akt signalni put ima biološku ulogu kao kritično-važni signalni put u delovanju adrenergičkih lekova, kao što je karvedilol, to ga čini ključnim za terapeutske intervencije u cilju minimalizacije ireverzibilnih tkivnih i ćelijskih oštećenja koja su asocirana sa HSI i hipertenzijom.
T2  - Materia medica
T1  - Effects of carvedilol on nitric oxide (NO) activity/expression in patient with chronic heart failure (CHF)
T1  - Efekti karvedilola na aktivnost/ekspresiju inducibilne azot oksid sintetaze (iNOS) kod bolesnika sa hroničnom srčanom insuficijencijom (HSI)
VL  - 24
IS  - 1
SP  - 21
EP  - 25
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10330
ER  - 

@article{
author = "Dobutović, Branislava and Trpković, Andreja and Putniković, Biljana and Gluvić, Zoran and Isenović, Esma R.",
year = "2008",
abstract = "Previous studies have reported increased myocardial inducible nitric oxide synthase (iNOs) expression and activity in chronic heart failure (ChF). Nitric oxide (NO) is a free radical which reacts with various molecules to cause multiple biological effects. Carvedilol is a α1-, β1-, and β2-adrenergic antagonist, used in therapy of hypertension and ChF. recently, it has been shown that carvedilol has an effect as NO quenching agent. Carvedilol presents several other mechanisms of action that converge to improve the symptomatology of hypertension and CHF. In addition to the adrenergic antagonism, carvedilol is also an antioxidant and endothelin suppressor. The molecular mechanism for the NO quenching potency of carvedilol remains to be determined. In cardiac cells the major pathway responsible for the regulation of iNOS activity/expression involves the activation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt). Thus, in our current ongoing and future studies, we will test the hypothesis that in disease states such as CHF where the PI3K/Akt pathway is interrupted, the regulation of iNOS activity/expression will be abolished. as a corollary of this primary hypothesis, we postulate that in CHF carvedilol stimulates cardiovascular iNOS via a mechanism involving activation of PI3K/akt cascade and further amplifies iNOS activity/expression. Moreover, since the PI3K/akt pathway have been acknowledged as a critically important mediator of cardiac iNOS regulation, PI3K/akt are identified as one of key targets for novel therapeutic interventions to minimize irreversible tissue damage associated with CHF and hypertension. A safer technology to regulate in vivo synthesis of PI3K/akt by generic manipulation would be a welcome work., Azot oksid (NO) je slobodni radikal čije reakcije dovode do različitih bioloških dejstava. Karvedilol je antagonist α1-, β1-,i β2 adrenergičkih receptora koji se koristi u terapiji hipertenzije i nedavno je pokazano da hemijski reaguje sa NO. Pored adrenergičke blokade karvedilol doprinosi poboljšanju hipertenzije i HSI drugim mehanizmima. Takođe, pokazano je da karvedilol ima ulogu antioksidansa i ulogu u supresiji endotelina. Precizan mehanizam interakcije karvedilola i NO do sada nije u potpunosti razjašnjen. aktivnost/ekspresija inducibilne azot oksid sintetaze (iNOS) u kardiomiocitima dominantno je regulisana aktivacijom fosfatidilinozitol 3-kinaze (PI3K) i protein kinaze B (akt). U našim tekućim i planiranim istraživanjima, polazimo od hipoteze da je u HSI poremećen PI3K/akt signalni put, a time konsekventno i smanjena aktivnost/ekspresija iNOS-a. Takođe, naša hipoteza se bazira na pretpostavci da karvedilol u HSI stimuliše iNOS u kardiovaskularnom sistemu preko aktivacije PI3K/Akt kaskade. U zaključku, regulacija PI3K/Akt signalnog puta ima veoma bitnu ulogu u regulaciji iNOS-a u stanjima HSI. S obzirom da PI3K/Akt signalni put ima biološku ulogu kao kritično-važni signalni put u delovanju adrenergičkih lekova, kao što je karvedilol, to ga čini ključnim za terapeutske intervencije u cilju minimalizacije ireverzibilnih tkivnih i ćelijskih oštećenja koja su asocirana sa HSI i hipertenzijom.",
journal = "Materia medica",
title = "Effects of carvedilol on nitric oxide (NO) activity/expression in patient with chronic heart failure (CHF), Efekti karvedilola na aktivnost/ekspresiju inducibilne azot oksid sintetaze (iNOS) kod bolesnika sa hroničnom srčanom insuficijencijom (HSI)",
volume = "24",
number = "1",
pages = "21-25",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10330"
}

Dobutović, B., Trpković, A., Putniković, B., Gluvić, Z.,& Isenović, E. R.. (2008). Effects of carvedilol on nitric oxide (NO) activity/expression in patient with chronic heart failure (CHF). in Materia medica, 24(1), 21-25.
https://hdl.handle.net/21.15107/rcub_vinar_10330

Dobutović B, Trpković A, Putniković B, Gluvić Z, Isenović ER. Effects of carvedilol on nitric oxide (NO) activity/expression in patient with chronic heart failure (CHF). in Materia medica. 2008;24(1):21-25.
https://hdl.handle.net/21.15107/rcub_vinar_10330 .

Dobutović, Branislava, Trpković, Andreja, Putniković, Biljana, Gluvić, Zoran, Isenović, Esma R., "Effects of carvedilol on nitric oxide (NO) activity/expression in patient with chronic heart failure (CHF)" in Materia medica, 24, no. 1 (2008):21-25,
https://hdl.handle.net/21.15107/rcub_vinar_10330 .

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Trpković, Andreja
AU  - Žakula, Zorica
AU  - Korićanac, Goran
AU  - Marche, Pierre
PY  - 2008
UR  - http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1573-4021&volume=4&issue=3&spage=190
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7803
AB  - It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. It is generally considered that the phosphorylation/dephosphorylation reactions of a variety of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including thrombin. ERK1/2 activation by G-protein-coupled receptors (GPCRs) has been shown to be Ca2--dependent and to require the transactivation of epidermal growth factor receptor (EGFR). In addition, it is generally admitted that variations of the intracellular Ca2- concentration ([Ca2-] i) play an important role in the transduction of mitogenic signal. Recently, we have shown that in thrombin-stimulated VSMCs, EGFR-independent activation of ERK1/2 activation could occur when agonist-induced ([Ca2-] i) elevation was reduced. This review examines recent findings in ERK1/2 signaling pathway that have been identified as critically important mediator of VSMCs hypertrophy and vascular diseases. Future investigations should now focus on the mechanisms of MAPK activation which might therefore represent a new mechanism involved in the antiproliferative effect revealed in this review.
T2  - Current Hypertension Reviews
T1  - Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy
VL  - 4
IS  - 3
SP  - 190
EP  - 196
DO  - 10.2174/157340208785132590
ER  - 

@article{
author = "Isenović, Esma R. and Trpković, Andreja and Žakula, Zorica and Korićanac, Goran and Marche, Pierre",
year = "2008",
abstract = "It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. It is generally considered that the phosphorylation/dephosphorylation reactions of a variety of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including thrombin. ERK1/2 activation by G-protein-coupled receptors (GPCRs) has been shown to be Ca2--dependent and to require the transactivation of epidermal growth factor receptor (EGFR). In addition, it is generally admitted that variations of the intracellular Ca2- concentration ([Ca2-] i) play an important role in the transduction of mitogenic signal. Recently, we have shown that in thrombin-stimulated VSMCs, EGFR-independent activation of ERK1/2 activation could occur when agonist-induced ([Ca2-] i) elevation was reduced. This review examines recent findings in ERK1/2 signaling pathway that have been identified as critically important mediator of VSMCs hypertrophy and vascular diseases. Future investigations should now focus on the mechanisms of MAPK activation which might therefore represent a new mechanism involved in the antiproliferative effect revealed in this review.",
journal = "Current Hypertension Reviews",
title = "Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy",
volume = "4",
number = "3",
pages = "190-196",
doi = "10.2174/157340208785132590"
}

Isenović, E. R., Trpković, A., Žakula, Z., Korićanac, G.,& Marche, P.. (2008). Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy. in Current Hypertension Reviews, 4(3), 190-196.
https://doi.org/10.2174/157340208785132590

Isenović ER, Trpković A, Žakula Z, Korićanac G, Marche P. Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy. in Current Hypertension Reviews. 2008;4(3):190-196.
doi:10.2174/157340208785132590 .

Isenović, Esma R., Trpković, Andreja, Žakula, Zorica, Korićanac, Goran, Marche, Pierre, "Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy" in Current Hypertension Reviews, 4, no. 3 (2008):190-196,
https://doi.org/10.2174/157340208785132590 . .

TY  - JOUR
AU  - Isenović, Esma R.
AU  - Trpković, Andreja
AU  - Žakula, Zorica
AU  - Korićanac, Goran
AU  - Marche, Pierre
PY  - 2008
UR  - http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1573-4021&volume=4&issue=3&spage=190
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7837
AB  - It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. It is generally considered that the phosphorylation/dephosphorylation reactions of a variety of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including thrombin. ERK1/2 activation by G-protein-coupled receptors (GPCRs) has been shown to be Ca2--dependent and to require the transactivation of epidermal growth factor receptor (EGFR). In addition, it is generally admitted that variations of the intracellular Ca2- concentration ([Ca2-] i) play an important role in the transduction of mitogenic signal. Recently, we have shown that in thrombin-stimulated VSMCs, EGFR-independent activation of ERK1/2 activation could occur when agonist-induced ([Ca2-] i) elevation was reduced. This review examines recent findings in ERK1/2 signaling pathway that have been identified as critically important mediator of VSMCs hypertrophy and vascular diseases. Future investigations should now focus on the mechanisms of MAPK activation which might therefore represent a new mechanism involved in the antiproliferative effect revealed in this review. © 2008 Bentham Science Publishers Ltd.
T2  - Current Hypertension Reviews
T1  - Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy
VL  - 4
IS  - 3
SP  - 190
EP  - 196
DO  - 10.2174/157340208785132590
ER  - 

@article{
author = "Isenović, Esma R. and Trpković, Andreja and Žakula, Zorica and Korićanac, Goran and Marche, Pierre",
year = "2008",
abstract = "It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. It is generally considered that the phosphorylation/dephosphorylation reactions of a variety of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including thrombin. ERK1/2 activation by G-protein-coupled receptors (GPCRs) has been shown to be Ca2--dependent and to require the transactivation of epidermal growth factor receptor (EGFR). In addition, it is generally admitted that variations of the intracellular Ca2- concentration ([Ca2-] i) play an important role in the transduction of mitogenic signal. Recently, we have shown that in thrombin-stimulated VSMCs, EGFR-independent activation of ERK1/2 activation could occur when agonist-induced ([Ca2-] i) elevation was reduced. This review examines recent findings in ERK1/2 signaling pathway that have been identified as critically important mediator of VSMCs hypertrophy and vascular diseases. Future investigations should now focus on the mechanisms of MAPK activation which might therefore represent a new mechanism involved in the antiproliferative effect revealed in this review. © 2008 Bentham Science Publishers Ltd.",
journal = "Current Hypertension Reviews",
title = "Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy",
volume = "4",
number = "3",
pages = "190-196",
doi = "10.2174/157340208785132590"
}

Isenović, E. R., Trpković, A., Žakula, Z., Korićanac, G.,& Marche, P.. (2008). Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy. in Current Hypertension Reviews, 4(3), 190-196.
https://doi.org/10.2174/157340208785132590

Isenović ER, Trpković A, Žakula Z, Korićanac G, Marche P. Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy. in Current Hypertension Reviews. 2008;4(3):190-196.
doi:10.2174/157340208785132590 .

Isenović, Esma R., Trpković, Andreja, Žakula, Zorica, Korićanac, Goran, Marche, Pierre, "Role of ERK1/2 Activation In Thrombin-Induced Vascular Smooth Muscle Cell Hypertrophy" in Current Hypertension Reviews, 4, no. 3 (2008):190-196,
https://doi.org/10.2174/157340208785132590 . .

TY  - JOUR
AU  - Trpković, Andreja
AU  - Putniković, Biljana
AU  - Sudar, Emina
AU  - Velebit, Jelena
AU  - Gluvić, Zoran
AU  - Ilić, Želmira
AU  - Đurić, Jovanka
AU  - Isenović, Esma R.
PY  - 2007
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10333
AB  - The effects of estradiol involve the activation of multiple signaling cascades, including and p42/44 mitogen-activated protein kinase. In addition, some of the effects of estradiol have been linked to activity of cytosolic phospholipase. The mechanisms of estradiol action on the cardiovascular system can be divided into two broad categories: effects on systemic cardiovascular risk factors, and direct effects on vascular cells. A number of direct vascular effects of estradiol have been reported, including its impact on the regulation of sodium pump activity and vasomotor tone. The sodium pump is a ubiquitous plasma membrane- bound enzyme that plays an essential role in regulatory vasomotion. The association between reduced sodium pump expression and the development and/or pathogenesis of several disease states including hypertension, congestive heart failure, chronic renal failure and diabetes underscores the importance of the sodium pump. We hypothesize that estradiol stimulates the vascular smooth muscle cell sodium pump via a mechanism involving phosphatydil inositol-3 kinase-dependent activation of cytosolic phospholipase and release of arachidonic acid , which activates the p42/44 mitogen-activated protein kinase cascade and further increases cytosolic phospholipase activity. Furthermore, we postulate that in a disease state such as hypertension (as in spontaneously hypertensive rat ), the resulting overproduction of Angiotensin II will interfere with estradiol regulation of the sodium pump.
AB  - Estradiol aktivira multipne kaskadne signalne reakcije u kojima su ukljuceni i enzimi, kinaze, kao sto su fosfatidil inozitol-3 kinaza i p42/44 mitogenom aktivirana kinaza. Takođe, se smatra da su pojedini efekti estradiola posledica aktivnosti citosolne fosfolipaze 2. Uticaj estradiola na kardiovaskularni sistem je dvojak: pored direktnog efekta na vaskularne ćelije, estradiol utiče i na sistemske faktore rizika koji dovode do pojave kardiovaskularne bolesti. Poznati su brojni direktni uticaji estradiola na vaskularni sistem, uključujući i ulogu estradiola u regulaciji aktivnosti natrijumove pumpe i vazomotornog tonusa. Natrijumova pumpa je ubikvitaran enzim lokalizovan u ćelijskoj membrani i ima značajnu ulogu u regulaciji vazomotornog tonusa. Poremecaj u regulaciji aktivnosti (npr. smanjena aktivnost), natrijumove pumpe je posebno izražena u nastanku i/ili patogenezi pojedinih oboljenja kao što su: hipertenzija, kongestivna srčana slabost, hronična bubrežna slabost i šećerna bolest. U nasem radu polazimo od hipoteze da estradiol stimuliše aktivnost/sintezu natrijumove pumpe u vaskularnim glatkim mišićnim ćelijama putem fosfatidil inozitol-3 kinazne-zavisne aktivacije citosolne fosfolipaze 2, nakon cega oslobođena arahidonska kiselina, indukuje aktivaciju p42/44 mitogenom aktiviriranu kinaznu kaskadnu reakciju sto dodatno doprinosi aktivnosti citosolne fosfolipaze 2.Takođe, smatramo da se u oboljenjima kao što je hipertenzija, povećana sinteza angiotenzina II ometa estradiolom regulisanu aktivnost/sintezu natrujumove pumpe.
T2  - Materia medica
T1  - Regulation of sodium pump by estradiol in vascular smooth muscle cells
T1  - Uloga estradiola u regulaciji netrijumove pumpe u vaskularnim glatkim mišićnim ćelijama
VL  - 23
IS  - 3
SP  - 32
EP  - 36
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10333
ER  - 

@article{
author = "Trpković, Andreja and Putniković, Biljana and Sudar, Emina and Velebit, Jelena and Gluvić, Zoran and Ilić, Želmira and Đurić, Jovanka and Isenović, Esma R.",
year = "2007",
abstract = "The effects of estradiol involve the activation of multiple signaling cascades, including and p42/44 mitogen-activated protein kinase. In addition, some of the effects of estradiol have been linked to activity of cytosolic phospholipase. The mechanisms of estradiol action on the cardiovascular system can be divided into two broad categories: effects on systemic cardiovascular risk factors, and direct effects on vascular cells. A number of direct vascular effects of estradiol have been reported, including its impact on the regulation of sodium pump activity and vasomotor tone. The sodium pump is a ubiquitous plasma membrane- bound enzyme that plays an essential role in regulatory vasomotion. The association between reduced sodium pump expression and the development and/or pathogenesis of several disease states including hypertension, congestive heart failure, chronic renal failure and diabetes underscores the importance of the sodium pump. We hypothesize that estradiol stimulates the vascular smooth muscle cell sodium pump via a mechanism involving phosphatydil inositol-3 kinase-dependent activation of cytosolic phospholipase and release of arachidonic acid , which activates the p42/44 mitogen-activated protein kinase cascade and further increases cytosolic phospholipase activity. Furthermore, we postulate that in a disease state such as hypertension (as in spontaneously hypertensive rat ), the resulting overproduction of Angiotensin II will interfere with estradiol regulation of the sodium pump., Estradiol aktivira multipne kaskadne signalne reakcije u kojima su ukljuceni i enzimi, kinaze, kao sto su fosfatidil inozitol-3 kinaza i p42/44 mitogenom aktivirana kinaza. Takođe, se smatra da su pojedini efekti estradiola posledica aktivnosti citosolne fosfolipaze 2. Uticaj estradiola na kardiovaskularni sistem je dvojak: pored direktnog efekta na vaskularne ćelije, estradiol utiče i na sistemske faktore rizika koji dovode do pojave kardiovaskularne bolesti. Poznati su brojni direktni uticaji estradiola na vaskularni sistem, uključujući i ulogu estradiola u regulaciji aktivnosti natrijumove pumpe i vazomotornog tonusa. Natrijumova pumpa je ubikvitaran enzim lokalizovan u ćelijskoj membrani i ima značajnu ulogu u regulaciji vazomotornog tonusa. Poremecaj u regulaciji aktivnosti (npr. smanjena aktivnost), natrijumove pumpe je posebno izražena u nastanku i/ili patogenezi pojedinih oboljenja kao što su: hipertenzija, kongestivna srčana slabost, hronična bubrežna slabost i šećerna bolest. U nasem radu polazimo od hipoteze da estradiol stimuliše aktivnost/sintezu natrijumove pumpe u vaskularnim glatkim mišićnim ćelijama putem fosfatidil inozitol-3 kinazne-zavisne aktivacije citosolne fosfolipaze 2, nakon cega oslobođena arahidonska kiselina, indukuje aktivaciju p42/44 mitogenom aktiviriranu kinaznu kaskadnu reakciju sto dodatno doprinosi aktivnosti citosolne fosfolipaze 2.Takođe, smatramo da se u oboljenjima kao što je hipertenzija, povećana sinteza angiotenzina II ometa estradiolom regulisanu aktivnost/sintezu natrujumove pumpe.",
journal = "Materia medica",
title = "Regulation of sodium pump by estradiol in vascular smooth muscle cells, Uloga estradiola u regulaciji netrijumove pumpe u vaskularnim glatkim mišićnim ćelijama",
volume = "23",
number = "3",
pages = "32-36",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10333"
}

Trpković, A., Putniković, B., Sudar, E., Velebit, J., Gluvić, Z., Ilić, Ž., Đurić, J.,& Isenović, E. R.. (2007). Regulation of sodium pump by estradiol in vascular smooth muscle cells. in Materia medica, 23(3), 32-36.
https://hdl.handle.net/21.15107/rcub_vinar_10333

Trpković A, Putniković B, Sudar E, Velebit J, Gluvić Z, Ilić Ž, Đurić J, Isenović ER. Regulation of sodium pump by estradiol in vascular smooth muscle cells. in Materia medica. 2007;23(3):32-36.
https://hdl.handle.net/21.15107/rcub_vinar_10333 .

Trpković, Andreja, Putniković, Biljana, Sudar, Emina, Velebit, Jelena, Gluvić, Zoran, Ilić, Želmira, Đurić, Jovanka, Isenović, Esma R., "Regulation of sodium pump by estradiol in vascular smooth muscle cells" in Materia medica, 23, no. 3 (2007):32-36,
https://hdl.handle.net/21.15107/rcub_vinar_10333 .