TY  - JOUR
AU  - Radak, Đorđe J.
AU  - Katsiki, Niki
AU  - Resanović, Ivana
AU  - Jovanović, Aleksandra
AU  - Sudar, Emina
AU  - Zafirović, Sonja
AU  - Mousa, Shaker A.
AU  - Isenović, Esma R.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1521
AB  - Apoptosis may contribute to a significant proportion of neuron death following acute brain ischemia (ABI), but the underlying mechanisms are still not fully understood. Brain ischemia may lead to stroke, which is one of the main causes of long-term morbidity and mortality in both developed and developing countries. Therefore, stroke prevention and treatment is clinically important. There are two important separate areas of the brain during ABI: the ischemic core and the ischemic penumbra. The ischemic core of the brain experiences a sudden reduction of blood flow, just minutes after ischemic attack with irreversible injury and subsequent cell death. On the other hand, apoptosis within the ischemic penumbra may occur after several hours or days, while necrosis starts in the first hours after the onset of ABI in the ischemic core. ABI is characterized by key molecular events that initiate apoptosis in many cells, such as overproduction of free radicals, Ca2+ overload and excitotoxicity. These changes in cellular homeostasis may trigger either necrosis or apoptosis, which often depends on cell type, cell age, and location in the brain. Apoptosis results in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. This review focuses on recent findings based on animal and human studies regarding the apoptotic mechanisms of neuronal death following ABI and the development of potential neuroprotective agents that reduce morbidity. The effects of statins on stroke prevention and treatment as well as on apoptotic mediators are also considered.
T2  - Current Vascular Pharmacology
T1  - Apoptosis and Acute Brain Ischemia in Ischemic Stroke
VL  - 15
IS  - 2
SP  - 115
EP  - 122
DO  - 10.2174/1570161115666161104095522
ER  - 

@article{
author = "Radak, Đorđe J. and Katsiki, Niki and Resanović, Ivana and Jovanović, Aleksandra and Sudar, Emina and Zafirović, Sonja and Mousa, Shaker A. and Isenović, Esma R.",
year = "2017",
abstract = "Apoptosis may contribute to a significant proportion of neuron death following acute brain ischemia (ABI), but the underlying mechanisms are still not fully understood. Brain ischemia may lead to stroke, which is one of the main causes of long-term morbidity and mortality in both developed and developing countries. Therefore, stroke prevention and treatment is clinically important. There are two important separate areas of the brain during ABI: the ischemic core and the ischemic penumbra. The ischemic core of the brain experiences a sudden reduction of blood flow, just minutes after ischemic attack with irreversible injury and subsequent cell death. On the other hand, apoptosis within the ischemic penumbra may occur after several hours or days, while necrosis starts in the first hours after the onset of ABI in the ischemic core. ABI is characterized by key molecular events that initiate apoptosis in many cells, such as overproduction of free radicals, Ca2+ overload and excitotoxicity. These changes in cellular homeostasis may trigger either necrosis or apoptosis, which often depends on cell type, cell age, and location in the brain. Apoptosis results in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. This review focuses on recent findings based on animal and human studies regarding the apoptotic mechanisms of neuronal death following ABI and the development of potential neuroprotective agents that reduce morbidity. The effects of statins on stroke prevention and treatment as well as on apoptotic mediators are also considered.",
journal = "Current Vascular Pharmacology",
title = "Apoptosis and Acute Brain Ischemia in Ischemic Stroke",
volume = "15",
number = "2",
pages = "115-122",
doi = "10.2174/1570161115666161104095522"
}

Radak, Đ. J., Katsiki, N., Resanović, I., Jovanović, A., Sudar, E., Zafirović, S., Mousa, S. A.,& Isenović, E. R.. (2017). Apoptosis and Acute Brain Ischemia in Ischemic Stroke. in Current Vascular Pharmacology, 15(2), 115-122.
https://doi.org/10.2174/1570161115666161104095522

Radak ĐJ, Katsiki N, Resanović I, Jovanović A, Sudar E, Zafirović S, Mousa SA, Isenović ER. Apoptosis and Acute Brain Ischemia in Ischemic Stroke. in Current Vascular Pharmacology. 2017;15(2):115-122.
doi:10.2174/1570161115666161104095522 .

Radak, Đorđe J., Katsiki, Niki, Resanović, Ivana, Jovanović, Aleksandra, Sudar, Emina, Zafirović, Sonja, Mousa, Shaker A., Isenović, Esma R., "Apoptosis and Acute Brain Ischemia in Ischemic Stroke" in Current Vascular Pharmacology, 15, no. 2 (2017):115-122,
https://doi.org/10.2174/1570161115666161104095522 . .

TY  - JOUR
AU  - Stanimirović, Julijana
AU  - Obradović, Milan M.
AU  - Zafirović, Sonja
AU  - Resanović, Ivana
AU  - Bogdanović, Nikola
AU  - Gluvić, Zoran
AU  - Mousa, Shaker A.
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/511
AB  - An altered hepatic lipid metabolism involves multifactorial pathologies such as hepatic inflammation, insulin resistance and oxidative stress. Immunity has an essential role in the regulation of glucose and lipid metabolism in the liver. Inducible nitric oxide (NO) synthase (iNOS) has been proposed as an important factor that interplays between immunity and energy metabolism and also in the pathogenesis of obesity-linked insulin resistance. In the liver, locally produced NO plays a protective role during inflammation, and the balance of NO protective and cytotoxic effects is very important. This review is focused on understanding the molecular mechanisms of iNOS regulation in the state of altered hepatic lipid metabolism, which is critical for developing new strategies for treatment of hepatic disorders.
T2  - Clinical Lipidology
T1  - Effects of altered hepatic lipid metabolism on regulation of hepatic iNOS
VL  - 10
IS  - 2
SP  - 167
EP  - 175
DO  - 10.2217/CLP.15.8
ER  - 

@article{
author = "Stanimirović, Julijana and Obradović, Milan M. and Zafirović, Sonja and Resanović, Ivana and Bogdanović, Nikola and Gluvić, Zoran and Mousa, Shaker A. and Isenović, Esma R.",
year = "2015",
abstract = "An altered hepatic lipid metabolism involves multifactorial pathologies such as hepatic inflammation, insulin resistance and oxidative stress. Immunity has an essential role in the regulation of glucose and lipid metabolism in the liver. Inducible nitric oxide (NO) synthase (iNOS) has been proposed as an important factor that interplays between immunity and energy metabolism and also in the pathogenesis of obesity-linked insulin resistance. In the liver, locally produced NO plays a protective role during inflammation, and the balance of NO protective and cytotoxic effects is very important. This review is focused on understanding the molecular mechanisms of iNOS regulation in the state of altered hepatic lipid metabolism, which is critical for developing new strategies for treatment of hepatic disorders.",
journal = "Clinical Lipidology",
title = "Effects of altered hepatic lipid metabolism on regulation of hepatic iNOS",
volume = "10",
number = "2",
pages = "167-175",
doi = "10.2217/CLP.15.8"
}

Stanimirović, J., Obradović, M. M., Zafirović, S., Resanović, I., Bogdanović, N., Gluvić, Z., Mousa, S. A.,& Isenović, E. R.. (2015). Effects of altered hepatic lipid metabolism on regulation of hepatic iNOS. in Clinical Lipidology, 10(2), 167-175.
https://doi.org/10.2217/CLP.15.8

Stanimirović J, Obradović MM, Zafirović S, Resanović I, Bogdanović N, Gluvić Z, Mousa SA, Isenović ER. Effects of altered hepatic lipid metabolism on regulation of hepatic iNOS. in Clinical Lipidology. 2015;10(2):167-175.
doi:10.2217/CLP.15.8 .

Stanimirović, Julijana, Obradović, Milan M., Zafirović, Sonja, Resanović, Ivana, Bogdanović, Nikola, Gluvić, Zoran, Mousa, Shaker A., Isenović, Esma R., "Effects of altered hepatic lipid metabolism on regulation of hepatic iNOS" in Clinical Lipidology, 10, no. 2 (2015):167-175,
https://doi.org/10.2217/CLP.15.8 . .

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  - Obradović, Milan M.
AU  - Zafirović, Sonja
AU  - Jovanović, Aleksandra
AU  - Sudar, Emina
AU  - Mousa, Shaker A.
AU  - Labudović-Borović, Milica
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/803
AB  - The aim of this study was to investigate in vivo effects of estradiol on Na+/K+-ATPase activity/expression in high fat (HF) diet fed rats. Adult male Wistar rats were fed normally (Control, n = 7) or with a HF diet (Obese, n = 14) for 10 weeks. After 10 weeks, half of the obese rats were treated with estradiol (Obese + Estradiol, n = 7, 40 mu g/kg, i.p.) as a bolus injection and 24 h after treatment all the rats were sacrificed. Estradiol in vivo in obese rats in comparison with obese non-treated rats led to a statistically significant increase in concentration of serum Na+ (p LT 0.05), Na+/K+-ATPase activity (p LT 0.01), expression of alpha 1 (p LT 0.01) and alpha 2 (p LT 0.05) subunit of Na+/K+-ATPase, both PI3K subunits p85 (p LT 0.01), p110 (p LT 0.05), and association of IRS-1 with p85 (p LT 0.05), while significantly decrease expression of AT1 (p LT 0.05) and Rho A (p LT 0.01) proteins. Our results suggest that estradiol in vivo in pathophysiological conditions, such as obesity accompanied with insulin resistance stimulates activity and expression of Na+/K+-ATPase by a mechanism that involves the participation of IRS-1/PI3K/Akt signaling. In addition, the decreasing level of AT1 and Rho A proteins estradiol probably attenuates the detrimental effect of obesity to decreased IRS-1/P13K association and consequently reduce Na+/K+-ATPase activity/expression. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
PB  - Elsevier
T2  - Molecular and Cellular Endocrinology
T1  - Effects of 17 beta-estradiol on cardiac Na+/K+-ATPase in high fat diet fed rats
VL  - 416
IS  - C
SP  - 46
EP  - 56
DO  - 10.1016/j.mce.2015.08.020
ER  - 

@article{
author = "Obradović, Milan M. and Zafirović, Sonja and Jovanović, Aleksandra and Sudar, Emina and Mousa, Shaker A. and Labudović-Borović, Milica and Isenović, Esma R.",
year = "2015",
abstract = "The aim of this study was to investigate in vivo effects of estradiol on Na+/K+-ATPase activity/expression in high fat (HF) diet fed rats. Adult male Wistar rats were fed normally (Control, n = 7) or with a HF diet (Obese, n = 14) for 10 weeks. After 10 weeks, half of the obese rats were treated with estradiol (Obese + Estradiol, n = 7, 40 mu g/kg, i.p.) as a bolus injection and 24 h after treatment all the rats were sacrificed. Estradiol in vivo in obese rats in comparison with obese non-treated rats led to a statistically significant increase in concentration of serum Na+ (p LT 0.05), Na+/K+-ATPase activity (p LT 0.01), expression of alpha 1 (p LT 0.01) and alpha 2 (p LT 0.05) subunit of Na+/K+-ATPase, both PI3K subunits p85 (p LT 0.01), p110 (p LT 0.05), and association of IRS-1 with p85 (p LT 0.05), while significantly decrease expression of AT1 (p LT 0.05) and Rho A (p LT 0.01) proteins. Our results suggest that estradiol in vivo in pathophysiological conditions, such as obesity accompanied with insulin resistance stimulates activity and expression of Na+/K+-ATPase by a mechanism that involves the participation of IRS-1/PI3K/Akt signaling. In addition, the decreasing level of AT1 and Rho A proteins estradiol probably attenuates the detrimental effect of obesity to decreased IRS-1/P13K association and consequently reduce Na+/K+-ATPase activity/expression. (C) 2015 Elsevier Ireland Ltd. All rights reserved.",
publisher = "Elsevier",
journal = "Molecular and Cellular Endocrinology",
title = "Effects of 17 beta-estradiol on cardiac Na+/K+-ATPase in high fat diet fed rats",
volume = "416",
number = "C",
pages = "46-56",
doi = "10.1016/j.mce.2015.08.020"
}

Obradović, M. M., Zafirović, S., Jovanović, A., Sudar, E., Mousa, S. A., Labudović-Borović, M.,& Isenović, E. R.. (2015). Effects of 17 beta-estradiol on cardiac Na+/K+-ATPase in high fat diet fed rats. in Molecular and Cellular Endocrinology
Elsevier., 416(C), 46-56.
https://doi.org/10.1016/j.mce.2015.08.020

Obradović MM, Zafirović S, Jovanović A, Sudar E, Mousa SA, Labudović-Borović M, Isenović ER. Effects of 17 beta-estradiol on cardiac Na+/K+-ATPase in high fat diet fed rats. in Molecular and Cellular Endocrinology. 2015;416(C):46-56.
doi:10.1016/j.mce.2015.08.020 .

Obradović, Milan M., Zafirović, Sonja, Jovanović, Aleksandra, Sudar, Emina, Mousa, Shaker A., Labudović-Borović, Milica, Isenović, Esma R., "Effects of 17 beta-estradiol on cardiac Na+/K+-ATPase in high fat diet fed rats" in Molecular and Cellular Endocrinology, 416, no. C (2015):46-56,
https://doi.org/10.1016/j.mce.2015.08.020 . .

TY  - JOUR
AU  - Stanekzai, Jamil
AU  - Isenović, Esma R.
AU  - Mousa, Shaker A.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5195
AB  - There are diseases and injuries in which a patients cells or tissues are destroyed that can only be adequately corrected by tissue or organ transplants. Stem cells may be able to generate new tissue and even cure diseases for which there is no adequate therapy. Type 1 diabetes (T1DM), an insulin-dependent diabetes, is a chronic disease affecting genetically predisposed individuals, in which insulin-secreting beta (beta)-cells within pancreatic islets of Langerhans are selectively and irreversibly destroyed by autoimmune assault. Type 2 diabetes (T2DM) is characterized by a gradual decrease in insulin sensitivity in peripheral tissues and the liver (insulin resistance), followed by a gradual decline in beta-cell function and insulin secretion. Successful replacing of damaged beta-cells has shown considerable potential in treating T1DM, but lack of adequate donors is a barrier. The literature suggests that embryonic and adult stem cells are promising alternatives in long-term treatment of diabetes. However, any successful strategy should address both the need for beta-cell replacement and controlling the autoimmune response to cells that express insulin. This review summarizes the current knowledge of options and the potential of stem cell transplantation in diabetes treatment. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
T2  - Diabetes Research and Clinical Practice
T1  - Treatment options for diabetes: Potential role of stem cells
VL  - 98
IS  - 3
SP  - 361
EP  - 368
DO  - 10.1016/j.diabres.2012.09.010
ER  - 

@article{
author = "Stanekzai, Jamil and Isenović, Esma R. and Mousa, Shaker A.",
year = "2012",
abstract = "There are diseases and injuries in which a patients cells or tissues are destroyed that can only be adequately corrected by tissue or organ transplants. Stem cells may be able to generate new tissue and even cure diseases for which there is no adequate therapy. Type 1 diabetes (T1DM), an insulin-dependent diabetes, is a chronic disease affecting genetically predisposed individuals, in which insulin-secreting beta (beta)-cells within pancreatic islets of Langerhans are selectively and irreversibly destroyed by autoimmune assault. Type 2 diabetes (T2DM) is characterized by a gradual decrease in insulin sensitivity in peripheral tissues and the liver (insulin resistance), followed by a gradual decline in beta-cell function and insulin secretion. Successful replacing of damaged beta-cells has shown considerable potential in treating T1DM, but lack of adequate donors is a barrier. The literature suggests that embryonic and adult stem cells are promising alternatives in long-term treatment of diabetes. However, any successful strategy should address both the need for beta-cell replacement and controlling the autoimmune response to cells that express insulin. This review summarizes the current knowledge of options and the potential of stem cell transplantation in diabetes treatment. (C) 2012 Elsevier Ireland Ltd. All rights reserved.",
journal = "Diabetes Research and Clinical Practice",
title = "Treatment options for diabetes: Potential role of stem cells",
volume = "98",
number = "3",
pages = "361-368",
doi = "10.1016/j.diabres.2012.09.010"
}

Stanekzai, J., Isenović, E. R.,& Mousa, S. A.. (2012). Treatment options for diabetes: Potential role of stem cells. in Diabetes Research and Clinical Practice, 98(3), 361-368.
https://doi.org/10.1016/j.diabres.2012.09.010

Stanekzai J, Isenović ER, Mousa SA. Treatment options for diabetes: Potential role of stem cells. in Diabetes Research and Clinical Practice. 2012;98(3):361-368.
doi:10.1016/j.diabres.2012.09.010 .

Stanekzai, Jamil, Isenović, Esma R., Mousa, Shaker A., "Treatment options for diabetes: Potential role of stem cells" in Diabetes Research and Clinical Practice, 98, no. 3 (2012):361-368,
https://doi.org/10.1016/j.diabres.2012.09.010 . .

TY  - JOUR
AU  - Haidara, Mohamed A.
AU  - Mikhailidis, Dimitri P.
AU  - Yassin, Hanaa Z.
AU  - Dobutović, Branislava
AU  - Smiljanić, Katarina
AU  - Soskić, Sanja S.
AU  - Mousa, Shaker A.
AU  - Rizzo, Manfredi
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4662
AB  - The metabolic syndrome (MetS) is common, and its associated risk burdens of diabetes and cardiovascular disease (CVD) are a major public health problem. The hypothesis that main constituent parameters of the MetS share common pathophysiologic mechanisms provides a conceptual framework for the future research. Exercise and weight loss can prevent insulin resistance and reduce the risk of diseases associated with the MetS. Interrupting intracellular and extracellular reactive oxygen species (ROS) overproduction could also contribute to normalizing the activation of metabolic pathways leading to the onset of diabetes, endothelial dysfunction, and cardiovascular (CV) complications. On the other hand, it is difficult to counteract the development of CV complications by using conventional antioxidants. Indeed, interest has focused on strategies that enhance the removal of ROS using either antioxidants or drugs that enhance endogenous antioxidant defense. Although these strategies have been effective in laboratory experiments, several clinical trials have shown that they do not reduce CV events, and in some cases antioxidants have actually worsened the outcome. More research is needed in this field.
T2  - Current Pharmaceutical Design
T1  - Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome
VL  - 17
IS  - 33
SP  - 3699
EP  - 3712
DO  - 10.2174/138161211798220882
ER  - 

@article{
author = "Haidara, Mohamed A. and Mikhailidis, Dimitri P. and Yassin, Hanaa Z. and Dobutović, Branislava and Smiljanić, Katarina and Soskić, Sanja S. and Mousa, Shaker A. and Rizzo, Manfredi and Isenović, Esma R.",
year = "2011",
abstract = "The metabolic syndrome (MetS) is common, and its associated risk burdens of diabetes and cardiovascular disease (CVD) are a major public health problem. The hypothesis that main constituent parameters of the MetS share common pathophysiologic mechanisms provides a conceptual framework for the future research. Exercise and weight loss can prevent insulin resistance and reduce the risk of diseases associated with the MetS. Interrupting intracellular and extracellular reactive oxygen species (ROS) overproduction could also contribute to normalizing the activation of metabolic pathways leading to the onset of diabetes, endothelial dysfunction, and cardiovascular (CV) complications. On the other hand, it is difficult to counteract the development of CV complications by using conventional antioxidants. Indeed, interest has focused on strategies that enhance the removal of ROS using either antioxidants or drugs that enhance endogenous antioxidant defense. Although these strategies have been effective in laboratory experiments, several clinical trials have shown that they do not reduce CV events, and in some cases antioxidants have actually worsened the outcome. More research is needed in this field.",
journal = "Current Pharmaceutical Design",
title = "Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome",
volume = "17",
number = "33",
pages = "3699-3712",
doi = "10.2174/138161211798220882"
}

Haidara, M. A., Mikhailidis, D. P., Yassin, H. Z., Dobutović, B., Smiljanić, K., Soskić, S. S., Mousa, S. A., Rizzo, M.,& Isenović, E. R.. (2011). Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome. in Current Pharmaceutical Design, 17(33), 3699-3712.
https://doi.org/10.2174/138161211798220882

Haidara MA, Mikhailidis DP, Yassin HZ, Dobutović B, Smiljanić K, Soskić SS, Mousa SA, Rizzo M, Isenović ER. Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome. in Current Pharmaceutical Design. 2011;17(33):3699-3712.
doi:10.2174/138161211798220882 .

Haidara, Mohamed A., Mikhailidis, Dimitri P., Yassin, Hanaa Z., Dobutović, Branislava, Smiljanić, Katarina, Soskić, Sanja S., Mousa, Shaker A., Rizzo, Manfredi, Isenović, Esma R., "Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome" in Current Pharmaceutical Design, 17, no. 33 (2011):3699-3712,
https://doi.org/10.2174/138161211798220882 . .