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  - Ilinčić, Branislava
AU  - Stokić, Edita
AU  - Stošić, Zoran
AU  - Kojić, Nevena Eremic
AU  - Katsiki, Niki
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1371
AB  - Introduction: Obesity and inadequate vitamin D status are associated with endothelial dysfunction and cardiovascular disease. We evaluated the associations between vitamin D status (i.e. serum levels of 25-hydroxyvitamin D (25(OH)D)), biomarkers of endothelial dysfunction (i.e. serum concentrations of soluble intercellular adhesion molecule 1 (sICAM-1) and soluble E-selectin (sE-selectin)), inflammatory markers (i.e. high-sensitivity C-reactive protein (hsCRP) and fibrinogen) and cardiometabolic risk factors. Material and methods: Fifty obese (body mass index (BMI) GT = 30 kg/m(2)) non-diabetic adults (mean age: 36.2 +/- 5.4 years) without pre-existing cardiovascular abnormalities and 25 clinically healthy, normal weight and age matched individuals were included. Anthropometric parameters, markers of glucose and lipid metabolism, and serum levels of inflammatory and endothelial dysfunction biomarkers were assessed in all subjects. Results: The mean serum 25(OH)D level was significantly lower in the obese group than in controls (33.5 +/- 15.2 vs. 60.1 +/- 23.1 nmol/l; p LT 0.001). In the obese group, sE-selectin (36.4 (32.1-47.2) vs. 32.4 (24.6-35.5) ng/ml, p LT 0.05) and hsCRP (6.0 +/- 3.4 vs. 3.5 1.0 mg/l, p LT 0.05) were significantly higher in individuals with lower than median vitamin D levels (i.e. 31 nmol/l) compared with those with higher vitamin D levels. In multivariable linear regression analysis, hsCRP (beta = 0.43; p LT 0.001) and sE-selectin (beta = 0.30; p = 0.03) were independently and significantly associated with serum 25(OH)D levels in the obese group. Conclusions: Vitamin D levels may be related to increased levels of biomarkers of endothelial dysfunction and inflammation in obese non-diabetic individuals.
T2  - Archives of Medical Science
T1  - Vitamin D status and circulating biomarkers of endothelial dysfunction and inflammation in non-diabetic obese individuals: a pilot study
VL  - 13
IS  - 1
SP  - 53
EP  - 60
DO  - 10.5114/aoms.2016.61812
ER  - 

@article{
author = "Ilinčić, Branislava and Stokić, Edita and Stošić, Zoran and Kojić, Nevena Eremic and Katsiki, Niki and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2017",
abstract = "Introduction: Obesity and inadequate vitamin D status are associated with endothelial dysfunction and cardiovascular disease. We evaluated the associations between vitamin D status (i.e. serum levels of 25-hydroxyvitamin D (25(OH)D)), biomarkers of endothelial dysfunction (i.e. serum concentrations of soluble intercellular adhesion molecule 1 (sICAM-1) and soluble E-selectin (sE-selectin)), inflammatory markers (i.e. high-sensitivity C-reactive protein (hsCRP) and fibrinogen) and cardiometabolic risk factors. Material and methods: Fifty obese (body mass index (BMI) GT = 30 kg/m(2)) non-diabetic adults (mean age: 36.2 +/- 5.4 years) without pre-existing cardiovascular abnormalities and 25 clinically healthy, normal weight and age matched individuals were included. Anthropometric parameters, markers of glucose and lipid metabolism, and serum levels of inflammatory and endothelial dysfunction biomarkers were assessed in all subjects. Results: The mean serum 25(OH)D level was significantly lower in the obese group than in controls (33.5 +/- 15.2 vs. 60.1 +/- 23.1 nmol/l; p LT 0.001). In the obese group, sE-selectin (36.4 (32.1-47.2) vs. 32.4 (24.6-35.5) ng/ml, p LT 0.05) and hsCRP (6.0 +/- 3.4 vs. 3.5 1.0 mg/l, p LT 0.05) were significantly higher in individuals with lower than median vitamin D levels (i.e. 31 nmol/l) compared with those with higher vitamin D levels. In multivariable linear regression analysis, hsCRP (beta = 0.43; p LT 0.001) and sE-selectin (beta = 0.30; p = 0.03) were independently and significantly associated with serum 25(OH)D levels in the obese group. Conclusions: Vitamin D levels may be related to increased levels of biomarkers of endothelial dysfunction and inflammation in obese non-diabetic individuals.",
journal = "Archives of Medical Science",
title = "Vitamin D status and circulating biomarkers of endothelial dysfunction and inflammation in non-diabetic obese individuals: a pilot study",
volume = "13",
number = "1",
pages = "53-60",
doi = "10.5114/aoms.2016.61812"
}

Ilinčić, B., Stokić, E., Stošić, Z., Kojić, N. E., Katsiki, N., Mikhailidis, D. P.,& Isenović, E. R.. (2017). Vitamin D status and circulating biomarkers of endothelial dysfunction and inflammation in non-diabetic obese individuals: a pilot study. in Archives of Medical Science, 13(1), 53-60.
https://doi.org/10.5114/aoms.2016.61812

Ilinčić B, Stokić E, Stošić Z, Kojić NE, Katsiki N, Mikhailidis DP, Isenović ER. Vitamin D status and circulating biomarkers of endothelial dysfunction and inflammation in non-diabetic obese individuals: a pilot study. in Archives of Medical Science. 2017;13(1):53-60.
doi:10.5114/aoms.2016.61812 .

Ilinčić, Branislava, Stokić, Edita, Stošić, Zoran, Kojić, Nevena Eremic, Katsiki, Niki, Mikhailidis, Dimitri P., Isenović, Esma R., "Vitamin D status and circulating biomarkers of endothelial dysfunction and inflammation in non-diabetic obese individuals: a pilot study" in Archives of Medical Science, 13, no. 1 (2017):53-60,
https://doi.org/10.5114/aoms.2016.61812 . .

TY  - JOUR
AU  - Rizzo, Manfredi
AU  - Obradović, Milan M.
AU  - Labudović-Borović, Milica
AU  - Nikolić, Dragana
AU  - Montalto, Giuseppe
AU  - Rizvi, Ali A.
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/290
AB  - In humans uric acid (UA) is the end product of degradation of purines. The handling of UA by the renal system is a complex process which is not fully understood. To date, several urate transporters in the renal proximal tubule have been identified. Among them, urate transporter 1 (URAT1) and a glucose transporter 9 (GLUT9) are considered of greater importance, as potential targets for treatment of hyperuricemia and the potential associated cardio-metabolic risk. Therefore, the recognition of the metabolic pathway of UA and elucidation of occurrence of hyperuricemia may provide important insights about the relationship between UA, pre-hypertension (preHT) and the metabolic syndrome (MetS). We also review the available clinical studies in this field, including experimental studies dealing with the mechanisms of UA transport via different transporters, as well as current treatment options for hyperuricemia in patients with MetS, preHT or cardiovascular risk factors.
T2  - Current Vascular Pharmacology
T1  - Uric Acid Metabolism in Pre-hypertension and the Metabolic Syndrome
VL  - 12
IS  - 4
SP  - 572
EP  - 585
DO  - 10.2174/1570161111999131205160756
ER  - 

@article{
author = "Rizzo, Manfredi and Obradović, Milan M. and Labudović-Borović, Milica and Nikolić, Dragana and Montalto, Giuseppe and Rizvi, Ali A. and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2014",
abstract = "In humans uric acid (UA) is the end product of degradation of purines. The handling of UA by the renal system is a complex process which is not fully understood. To date, several urate transporters in the renal proximal tubule have been identified. Among them, urate transporter 1 (URAT1) and a glucose transporter 9 (GLUT9) are considered of greater importance, as potential targets for treatment of hyperuricemia and the potential associated cardio-metabolic risk. Therefore, the recognition of the metabolic pathway of UA and elucidation of occurrence of hyperuricemia may provide important insights about the relationship between UA, pre-hypertension (preHT) and the metabolic syndrome (MetS). We also review the available clinical studies in this field, including experimental studies dealing with the mechanisms of UA transport via different transporters, as well as current treatment options for hyperuricemia in patients with MetS, preHT or cardiovascular risk factors.",
journal = "Current Vascular Pharmacology",
title = "Uric Acid Metabolism in Pre-hypertension and the Metabolic Syndrome",
volume = "12",
number = "4",
pages = "572-585",
doi = "10.2174/1570161111999131205160756"
}

Rizzo, M., Obradović, M. M., Labudović-Borović, M., Nikolić, D., Montalto, G., Rizvi, A. A., Mikhailidis, D. P.,& Isenović, E. R.. (2014). Uric Acid Metabolism in Pre-hypertension and the Metabolic Syndrome. in Current Vascular Pharmacology, 12(4), 572-585.
https://doi.org/10.2174/1570161111999131205160756

Rizzo M, Obradović MM, Labudović-Borović M, Nikolić D, Montalto G, Rizvi AA, Mikhailidis DP, Isenović ER. Uric Acid Metabolism in Pre-hypertension and the Metabolic Syndrome. in Current Vascular Pharmacology. 2014;12(4):572-585.
doi:10.2174/1570161111999131205160756 .

Rizzo, Manfredi, Obradović, Milan M., Labudović-Borović, Milica, Nikolić, Dragana, Montalto, Giuseppe, Rizvi, Ali A., Mikhailidis, Dimitri P., Isenović, Esma R., "Uric Acid Metabolism in Pre-hypertension and the Metabolic Syndrome" in Current Vascular Pharmacology, 12, no. 4 (2014):572-585,
https://doi.org/10.2174/1570161111999131205160756 . .

TY  - JOUR
AU  - Nikolić, Dragana
AU  - Katsiki, Niki
AU  - Montalto, Giuseppe
AU  - Isenović, Esma R.
AU  - Mikhailidis, Dimitri P.
AU  - Rizzo, Manfredi
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5380
AB  - Small, dense low density lipoprotein (sdLDL) represents an emerging cardiovascular risk factor, since these particles can be associated with cardiovascular disease (CVD) independently of established risk factors, including plasma lipids. Obese subjects frequently have atherogenic dyslipidaemia, including elevated sdLDL levels, in addition to elevated triglycerides (TG), very low density lipoprotein (VLDL) and apolipoprotein-B, as well as decreased high density lipoprotein cholesterol (HDL-C) levels. Obesity-related co-morbidities, such as metabolic syndrome (MetS) are also characterized by dyslipidaemia. Therefore, agents that favourably modulate LDL subclasses may be of clinical value in these subjects. Statins are the lipid-lowering drug of choice. Also, anti-obesity and lipid lowering drugs other than statins could be useful in these patients. However, the effects of anti-obesity drugs on CVD risk factors remain unclear. We review the clinical significance of sdLDL in being overweight and obesity, as well as the efficacy of anti-obesity drugs on LDL subfractions in these individuals; a short comment on HDL subclasses is also included. Our literature search was based on PubMed and Scopus listings. Further research is required to fully explore both the significance of sdLDL and the efficacy of anti-obesity drugs on LDL subfractions in being overweight, obesity and MetS. Improving the lipoprotein profile in these patients may represent an efficient approach for reducing cardiovascular risk.
T2  - Nutrients
T1  - Lipoprotein Subfractions in Metabolic Syndrome and Obesity: Clinical Significance and Therapeutic Approaches
VL  - 5
IS  - 3
SP  - 928
EP  - 948
DO  - 10.3390/nu5030928
ER  - 

@article{
author = "Nikolić, Dragana and Katsiki, Niki and Montalto, Giuseppe and Isenović, Esma R. and Mikhailidis, Dimitri P. and Rizzo, Manfredi",
year = "2013",
abstract = "Small, dense low density lipoprotein (sdLDL) represents an emerging cardiovascular risk factor, since these particles can be associated with cardiovascular disease (CVD) independently of established risk factors, including plasma lipids. Obese subjects frequently have atherogenic dyslipidaemia, including elevated sdLDL levels, in addition to elevated triglycerides (TG), very low density lipoprotein (VLDL) and apolipoprotein-B, as well as decreased high density lipoprotein cholesterol (HDL-C) levels. Obesity-related co-morbidities, such as metabolic syndrome (MetS) are also characterized by dyslipidaemia. Therefore, agents that favourably modulate LDL subclasses may be of clinical value in these subjects. Statins are the lipid-lowering drug of choice. Also, anti-obesity and lipid lowering drugs other than statins could be useful in these patients. However, the effects of anti-obesity drugs on CVD risk factors remain unclear. We review the clinical significance of sdLDL in being overweight and obesity, as well as the efficacy of anti-obesity drugs on LDL subfractions in these individuals; a short comment on HDL subclasses is also included. Our literature search was based on PubMed and Scopus listings. Further research is required to fully explore both the significance of sdLDL and the efficacy of anti-obesity drugs on LDL subfractions in being overweight, obesity and MetS. Improving the lipoprotein profile in these patients may represent an efficient approach for reducing cardiovascular risk.",
journal = "Nutrients",
title = "Lipoprotein Subfractions in Metabolic Syndrome and Obesity: Clinical Significance and Therapeutic Approaches",
volume = "5",
number = "3",
pages = "928-948",
doi = "10.3390/nu5030928"
}

Nikolić, D., Katsiki, N., Montalto, G., Isenović, E. R., Mikhailidis, D. P.,& Rizzo, M.. (2013). Lipoprotein Subfractions in Metabolic Syndrome and Obesity: Clinical Significance and Therapeutic Approaches. in Nutrients, 5(3), 928-948.
https://doi.org/10.3390/nu5030928

Nikolić D, Katsiki N, Montalto G, Isenović ER, Mikhailidis DP, Rizzo M. Lipoprotein Subfractions in Metabolic Syndrome and Obesity: Clinical Significance and Therapeutic Approaches. in Nutrients. 2013;5(3):928-948.
doi:10.3390/nu5030928 .

Nikolić, Dragana, Katsiki, Niki, Montalto, Giuseppe, Isenović, Esma R., Mikhailidis, Dimitri P., Rizzo, Manfredi, "Lipoprotein Subfractions in Metabolic Syndrome and Obesity: Clinical Significance and Therapeutic Approaches" in Nutrients, 5, no. 3 (2013):928-948,
https://doi.org/10.3390/nu5030928 . .

TY  - JOUR
AU  - Banach, Maciej
AU  - Rizzo, Manfredi
AU  - Obradović, Milan M.
AU  - Montalto, Giuseppe
AU  - Rysz, Jacek
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5502
AB  - Plasma low-density lipoprotein cholesterol (LDL-C) is one of the biomarkers of cardiovascular disease (CVD) risk. LDL is cleared from the circulation preferentially through the LDL receptor (LDLR) pathway. Proprotein convertase subtilisin/kexin 9 (PCSK9) promotes the degradation of the LDLR. PCSK9 inhibition is attractive as a new strategy for lowering LDL-C levels, especially in combination with lipid lowering drugs such as statins. We review data from the available studies which focus on PCSK9 as a potential target in the treatment of hyperlipidemia. Further studies are still necessary to investigate the potential underlying mechanisms involved.
T2  - Current Pharmaceutical Design
T1  - PCSK9 Inhibition - A Novel Mechanism to Treat Lipid Disorders?
VL  - 19
IS  - 21
SP  - 3869
EP  - 3877
DO  - 10.2174/13816128113199990303
ER  - 

@article{
author = "Banach, Maciej and Rizzo, Manfredi and Obradović, Milan M. and Montalto, Giuseppe and Rysz, Jacek and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2013",
abstract = "Plasma low-density lipoprotein cholesterol (LDL-C) is one of the biomarkers of cardiovascular disease (CVD) risk. LDL is cleared from the circulation preferentially through the LDL receptor (LDLR) pathway. Proprotein convertase subtilisin/kexin 9 (PCSK9) promotes the degradation of the LDLR. PCSK9 inhibition is attractive as a new strategy for lowering LDL-C levels, especially in combination with lipid lowering drugs such as statins. We review data from the available studies which focus on PCSK9 as a potential target in the treatment of hyperlipidemia. Further studies are still necessary to investigate the potential underlying mechanisms involved.",
journal = "Current Pharmaceutical Design",
title = "PCSK9 Inhibition - A Novel Mechanism to Treat Lipid Disorders?",
volume = "19",
number = "21",
pages = "3869-3877",
doi = "10.2174/13816128113199990303"
}

Banach, M., Rizzo, M., Obradović, M. M., Montalto, G., Rysz, J., Mikhailidis, D. P.,& Isenović, E. R.. (2013). PCSK9 Inhibition - A Novel Mechanism to Treat Lipid Disorders?. in Current Pharmaceutical Design, 19(21), 3869-3877.
https://doi.org/10.2174/13816128113199990303

Banach M, Rizzo M, Obradović MM, Montalto G, Rysz J, Mikhailidis DP, Isenović ER. PCSK9 Inhibition - A Novel Mechanism to Treat Lipid Disorders?. in Current Pharmaceutical Design. 2013;19(21):3869-3877.
doi:10.2174/13816128113199990303 .

Banach, Maciej, Rizzo, Manfredi, Obradović, Milan M., Montalto, Giuseppe, Rysz, Jacek, Mikhailidis, Dimitri P., Isenović, Esma R., "PCSK9 Inhibition - A Novel Mechanism to Treat Lipid Disorders?" in Current Pharmaceutical Design, 19, no. 21 (2013):3869-3877,
https://doi.org/10.2174/13816128113199990303 . .

TY  - JOUR
AU  - Rizzo, Manfredi
AU  - Rizvi, Ali A.
AU  - Sudar, Emina
AU  - Soskić, Sanja S.
AU  - Obradović, Milan M.
AU  - Montalto, Giuseppe
AU  - Boutjdir, Mohamed
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5565
AB  - Ghrelin is a peptide hormone produced mainly in the stomach that has widespread tissue distribution and diverse hormonal, metabolic and cardiovascular activities. The circulating ghrelin concentration increases during fasting and decreases after food intake. Ghrelin secretion may thus be initiated by food intake and is possibly controlled by nutritional factors. Lean subjects have increased levels of circulating ghrelin compared with obese subjects. Recent reports show that low plasma ghrelin is associated with elevated fasting insulin levels, insulin resistance and type 2 diabetes mellitus. Factors involved in the regulation of ghrelin secretion have not yet been defined; however, it is assumed that blood glucose levels represent a significant regulator. Recent evidence indicates that ghrelin can increase myocardial contractility, enhance vasodilatation, and has protective effect from myocardial damage. It has been shown that ghrelin may improve cardiac function through growth hormone (GH)-dependent mechanisms but there is also evidence to suggest that ghrelins cardioprotective activity is independent of GH. Recent data demonstrate that ghrelin can influence key events in atherogenesis. Thus, ghrelin may be a new target for the treatment of some cardiovascular diseases. In this review, we consider the current literature focusing on ghrelin as a potential antiatherogenic agent in the treatment of various pathophysiological conditions.
T2  - Current Pharmaceutical Design
T1  - A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin
VL  - 19
IS  - 27
SP  - 4953
EP  - 4963
DO  - 10.2174/1381612811319270018
ER  - 

@article{
author = "Rizzo, Manfredi and Rizvi, Ali A. and Sudar, Emina and Soskić, Sanja S. and Obradović, Milan M. and Montalto, Giuseppe and Boutjdir, Mohamed and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2013",
abstract = "Ghrelin is a peptide hormone produced mainly in the stomach that has widespread tissue distribution and diverse hormonal, metabolic and cardiovascular activities. The circulating ghrelin concentration increases during fasting and decreases after food intake. Ghrelin secretion may thus be initiated by food intake and is possibly controlled by nutritional factors. Lean subjects have increased levels of circulating ghrelin compared with obese subjects. Recent reports show that low plasma ghrelin is associated with elevated fasting insulin levels, insulin resistance and type 2 diabetes mellitus. Factors involved in the regulation of ghrelin secretion have not yet been defined; however, it is assumed that blood glucose levels represent a significant regulator. Recent evidence indicates that ghrelin can increase myocardial contractility, enhance vasodilatation, and has protective effect from myocardial damage. It has been shown that ghrelin may improve cardiac function through growth hormone (GH)-dependent mechanisms but there is also evidence to suggest that ghrelins cardioprotective activity is independent of GH. Recent data demonstrate that ghrelin can influence key events in atherogenesis. Thus, ghrelin may be a new target for the treatment of some cardiovascular diseases. In this review, we consider the current literature focusing on ghrelin as a potential antiatherogenic agent in the treatment of various pathophysiological conditions.",
journal = "Current Pharmaceutical Design",
title = "A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin",
volume = "19",
number = "27",
pages = "4953-4963",
doi = "10.2174/1381612811319270018"
}

Rizzo, M., Rizvi, A. A., Sudar, E., Soskić, S. S., Obradović, M. M., Montalto, G., Boutjdir, M., Mikhailidis, D. P.,& Isenović, E. R.. (2013). A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin. in Current Pharmaceutical Design, 19(27), 4953-4963.
https://doi.org/10.2174/1381612811319270018

Rizzo M, Rizvi AA, Sudar E, Soskić SS, Obradović MM, Montalto G, Boutjdir M, Mikhailidis DP, Isenović ER. A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin. in Current Pharmaceutical Design. 2013;19(27):4953-4963.
doi:10.2174/1381612811319270018 .

Rizzo, Manfredi, Rizvi, Ali A., Sudar, Emina, Soskić, Sanja S., Obradović, Milan M., Montalto, Giuseppe, Boutjdir, Mohamed, Mikhailidis, Dimitri P., Isenović, Esma R., "A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin" in Current Pharmaceutical Design, 19, no. 27 (2013):4953-4963,
https://doi.org/10.2174/1381612811319270018 . .

TY  - CHAP
AU  - Sudar, Emina
AU  - Soskić, Sanja S.
AU  - Zarić, Božidarka
AU  - Rašić-Milutinović, Zorica
AU  - Smiljanić, Katarina
AU  - Radak, Đorđe J.
AU  - Mikhailidis, Dimitri P.
AU  - Rizzo, Manfredi
AU  - Isenović, Esma R.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8685
AB  - Cardiovascular disease (CVD) is common cause of death in humans and its major underlying pathology is atherosclerosis. Atherosclerosis is a chronic inflammatory disease that predisposes to coronary artery disease (CAD), stroke and peripheral arterial disease, responsible for most of the cardiovascular morbidity and mortality. This inflammatory process, triggered by the presence of lipids in the vascular wall, and encompasses a complex interaction among inflammatory cells, vascular elements, and lipoproteins through the expression of several adhesion molecules and cytokines. Obesity is a risk factor for CVD but this association is not fully understood. Altered levels of obesity related peptides such as ghrelin may play an important role in this pathophysiology. Recent evidence indicates that ghrelin features several cardiovascular activities, including increased myocardial contractility, vasodilatation and protection from myocardial infarction. Recent data demonstrate that ghrelin can influence important key events in atherogenesis and thus they may play a role in atherosclerosis. In this review we present the latest data from recent animal and clinical studies which focus on a novel approach to ghrelin as a potential therapeutic agent in the treatment of a complex disease like atherosclerosis. Thus, ghrelin may become a new therapeutic target for the treatment of CVD. Further studies are necessary to investigate the potential mechanisms involved in the effects of ghrelin on the cardiovascular system.
T2  - Ghrelin: Production, Action Mechanisms and Physiological Effects
T1  - Ghrelin, obesity and atherosclerosis
SP  - 111
EP  - 126
UR  - https://hdl.handle.net/21.15107/rcub_vinar_8685
ER  - 

@inbook{
author = "Sudar, Emina and Soskić, Sanja S. and Zarić, Božidarka and Rašić-Milutinović, Zorica and Smiljanić, Katarina and Radak, Đorđe J. and Mikhailidis, Dimitri P. and Rizzo, Manfredi and Isenović, Esma R.",
year = "2012",
abstract = "Cardiovascular disease (CVD) is common cause of death in humans and its major underlying pathology is atherosclerosis. Atherosclerosis is a chronic inflammatory disease that predisposes to coronary artery disease (CAD), stroke and peripheral arterial disease, responsible for most of the cardiovascular morbidity and mortality. This inflammatory process, triggered by the presence of lipids in the vascular wall, and encompasses a complex interaction among inflammatory cells, vascular elements, and lipoproteins through the expression of several adhesion molecules and cytokines. Obesity is a risk factor for CVD but this association is not fully understood. Altered levels of obesity related peptides such as ghrelin may play an important role in this pathophysiology. Recent evidence indicates that ghrelin features several cardiovascular activities, including increased myocardial contractility, vasodilatation and protection from myocardial infarction. Recent data demonstrate that ghrelin can influence important key events in atherogenesis and thus they may play a role in atherosclerosis. In this review we present the latest data from recent animal and clinical studies which focus on a novel approach to ghrelin as a potential therapeutic agent in the treatment of a complex disease like atherosclerosis. Thus, ghrelin may become a new therapeutic target for the treatment of CVD. Further studies are necessary to investigate the potential mechanisms involved in the effects of ghrelin on the cardiovascular system.",
journal = "Ghrelin: Production, Action Mechanisms and Physiological Effects",
booktitle = "Ghrelin, obesity and atherosclerosis",
pages = "111-126",
url = "https://hdl.handle.net/21.15107/rcub_vinar_8685"
}

Sudar, E., Soskić, S. S., Zarić, B., Rašić-Milutinović, Z., Smiljanić, K., Radak, Đ. J., Mikhailidis, D. P., Rizzo, M.,& Isenović, E. R.. (2012). Ghrelin, obesity and atherosclerosis. in Ghrelin: Production, Action Mechanisms and Physiological Effects, 111-126.
https://hdl.handle.net/21.15107/rcub_vinar_8685

Sudar E, Soskić SS, Zarić B, Rašić-Milutinović Z, Smiljanić K, Radak ĐJ, Mikhailidis DP, Rizzo M, Isenović ER. Ghrelin, obesity and atherosclerosis. in Ghrelin: Production, Action Mechanisms and Physiological Effects. 2012;:111-126.
https://hdl.handle.net/21.15107/rcub_vinar_8685 .

Sudar, Emina, Soskić, Sanja S., Zarić, Božidarka, Rašić-Milutinović, Zorica, Smiljanić, Katarina, Radak, Đorđe J., Mikhailidis, Dimitri P., Rizzo, Manfredi, Isenović, Esma R., "Ghrelin, obesity and atherosclerosis" in Ghrelin: Production, Action Mechanisms and Physiological Effects (2012):111-126,
https://hdl.handle.net/21.15107/rcub_vinar_8685 .

TY  - JOUR
AU  - Bojić, Tijana
AU  - Sudar, Emina
AU  - Mikhailidis, Dimitri P.
AU  - Alavantić, Dragan
AU  - Isenović, Esma R.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5232
AB  - In coronary artery disease the G protein related kinases (GRKs) play a role in desensitization of beta-adrenoreceptors (AR) after coronary occlusion. Targeted deletion and lowering of cardiac myocyte GRK-2 decreases the risk of post-ischemic heart failure (HF). Studies carried out in humans confirm the role of GRK-2 as a marker for the progression of HF after myocardial infarction (MI). The level of GRK-2 could be an indicator of beta-AR blocker efficacy in patients with acute coronary syndrome. Elevated levels of GRK-2 are an early ubiquitous consequence of myocardial injury. In hypertension an increased level of GRK-2 was reported in both animal models and human studies. The role of GRKs in vagally mediated disorders such as vasovagal syncope and atrial fibrillation remains controversial. The role of GRKs in the pathogenesis of neurocardiological diseases provides an insight into the molecular pathogenesis process, opens potential therapeutic options and suggests new directions for scientific research.
T2  - Archives of Medical Science
T1  - The role of G protein coupled receptor kinases in neurocardiovascular pathophysiology
VL  - 8
IS  - 6
SP  - 970
EP  - 977
DO  - 10.5114/aoms.2012.32466
ER  - 

@article{
author = "Bojić, Tijana and Sudar, Emina and Mikhailidis, Dimitri P. and Alavantić, Dragan and Isenović, Esma R.",
year = "2012",
abstract = "In coronary artery disease the G protein related kinases (GRKs) play a role in desensitization of beta-adrenoreceptors (AR) after coronary occlusion. Targeted deletion and lowering of cardiac myocyte GRK-2 decreases the risk of post-ischemic heart failure (HF). Studies carried out in humans confirm the role of GRK-2 as a marker for the progression of HF after myocardial infarction (MI). The level of GRK-2 could be an indicator of beta-AR blocker efficacy in patients with acute coronary syndrome. Elevated levels of GRK-2 are an early ubiquitous consequence of myocardial injury. In hypertension an increased level of GRK-2 was reported in both animal models and human studies. The role of GRKs in vagally mediated disorders such as vasovagal syncope and atrial fibrillation remains controversial. The role of GRKs in the pathogenesis of neurocardiological diseases provides an insight into the molecular pathogenesis process, opens potential therapeutic options and suggests new directions for scientific research.",
journal = "Archives of Medical Science",
title = "The role of G protein coupled receptor kinases in neurocardiovascular pathophysiology",
volume = "8",
number = "6",
pages = "970-977",
doi = "10.5114/aoms.2012.32466"
}

Bojić, T., Sudar, E., Mikhailidis, D. P., Alavantić, D.,& Isenović, E. R.. (2012). The role of G protein coupled receptor kinases in neurocardiovascular pathophysiology. in Archives of Medical Science, 8(6), 970-977.
https://doi.org/10.5114/aoms.2012.32466

Bojić T, Sudar E, Mikhailidis DP, Alavantić D, Isenović ER. The role of G protein coupled receptor kinases in neurocardiovascular pathophysiology. in Archives of Medical Science. 2012;8(6):970-977.
doi:10.5114/aoms.2012.32466 .

Bojić, Tijana, Sudar, Emina, Mikhailidis, Dimitri P., Alavantić, Dragan, Isenović, Esma R., "The role of G protein coupled receptor kinases in neurocardiovascular pathophysiology" in Archives of Medical Science, 8, no. 6 (2012):970-977,
https://doi.org/10.5114/aoms.2012.32466 . .

TY  - JOUR
AU  - Soskić, Sanja S.
AU  - Dobutović, Branislava
AU  - Sudar, Emina
AU  - Obradović, Milan M.
AU  - Nikolić, Dragana
AU  - Zarić, Božidarka
AU  - Stojanovic, Srdan D.
AU  - Stokić, Edita
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4519
AB  - The peroxisome proliferator-activated receptors (PPARs) represent the family of 3 nuclear receptor isoforms-PPAR alpha, -gamma, and -delta/beta, which are encoded by different genes. As lipid sensors, they are primarily involved in regulation of lipid metabolism and subsequently in inflammation and atherosclerosis. Atherosclerosis considers accumulation of the cells and extracellular matrix in the vessel wall leading to the formation of atherosclerotic plaque, atherothrombosis, and other vascular complications. Besides existence of natural ligands for PPARs, their more potent synthetic ligands are fibrates and thiazolidindiones. Future investigations should now focus on the mechanisms of PPARs activation, which might present new approaches involved in the antiatherosclerotic effects revealed in this review. In addition, in this review we are presenting latest data from recent performed clinical studies which have focus on novel approach to PPARs agonists as potential therapeutic agents in the treatment of complex disease such as atherosclerosis.
T2  - Angiology
T1  - Peroxisome Proliferator-Activated Receptors and Atherosclerosis
VL  - 62
IS  - 7
SP  - 523
EP  - 534
DO  - 10.1177/0003319711401012
ER  - 

@article{
author = "Soskić, Sanja S. and Dobutović, Branislava and Sudar, Emina and Obradović, Milan M. and Nikolić, Dragana and Zarić, Božidarka and Stojanovic, Srdan D. and Stokić, Edita and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2011",
abstract = "The peroxisome proliferator-activated receptors (PPARs) represent the family of 3 nuclear receptor isoforms-PPAR alpha, -gamma, and -delta/beta, which are encoded by different genes. As lipid sensors, they are primarily involved in regulation of lipid metabolism and subsequently in inflammation and atherosclerosis. Atherosclerosis considers accumulation of the cells and extracellular matrix in the vessel wall leading to the formation of atherosclerotic plaque, atherothrombosis, and other vascular complications. Besides existence of natural ligands for PPARs, their more potent synthetic ligands are fibrates and thiazolidindiones. Future investigations should now focus on the mechanisms of PPARs activation, which might present new approaches involved in the antiatherosclerotic effects revealed in this review. In addition, in this review we are presenting latest data from recent performed clinical studies which have focus on novel approach to PPARs agonists as potential therapeutic agents in the treatment of complex disease such as atherosclerosis.",
journal = "Angiology",
title = "Peroxisome Proliferator-Activated Receptors and Atherosclerosis",
volume = "62",
number = "7",
pages = "523-534",
doi = "10.1177/0003319711401012"
}

Soskić, S. S., Dobutović, B., Sudar, E., Obradović, M. M., Nikolić, D., Zarić, B., Stojanovic, S. D., Stokić, E., Mikhailidis, D. P.,& Isenović, E. R.. (2011). Peroxisome Proliferator-Activated Receptors and Atherosclerosis. in Angiology, 62(7), 523-534.
https://doi.org/10.1177/0003319711401012

Soskić SS, Dobutović B, Sudar E, Obradović MM, Nikolić D, Zarić B, Stojanovic SD, Stokić E, Mikhailidis DP, Isenović ER. Peroxisome Proliferator-Activated Receptors and Atherosclerosis. in Angiology. 2011;62(7):523-534.
doi:10.1177/0003319711401012 .

Soskić, Sanja S., Dobutović, Branislava, Sudar, Emina, Obradović, Milan M., Nikolić, Dragana, Zarić, Božidarka, Stojanovic, Srdan D., Stokić, Edita, Mikhailidis, Dimitri P., Isenović, Esma R., "Peroxisome Proliferator-Activated Receptors and Atherosclerosis" in Angiology, 62, no. 7 (2011):523-534,
https://doi.org/10.1177/0003319711401012 . .

TY  - JOUR
AU  - Sudar, Emina
AU  - Dobutović, Branislava
AU  - Soskić, Sanja S.
AU  - Mandušić, Vesna
AU  - Žakula, Zorica
AU  - Misirkić, Maja
AU  - Vucicevic, Ljubica
AU  - Janjetović, Kristina D.
AU  - Trajković, Vladimir S.
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4317
AB  - The purpose of this study was to examine the effects of ghrelin on protein kinase B (Akt) and mitogen-activated protein kinase p42/44 (ERK1/2) activation as well as ghrelin effects on inducible nitric oxide (NO) synthase (iNOS; for gene Nos2) activity/expression in rat hearts. Male Wistar rats were treated with ghrelin (0.3 nmol/5 mu l) or an equal volume of phosphate-buffered saline, injected every 24 h into the lateral cerebral ventricle for 5 days and 2 h after the last treatment the animals were sacrificed. Serum NO, l-arginine (l-Arg), and arginase activity were measured spectrophotometrically. For phosphorylation of Akt, ERK1/2, and iNOS protein expression, Western blot method was used. The expression of Nos2 mRNA was measured by the quantitative real-time polymerase chain reaction (qRT-PCR). Treatment with ghrelin significantly increased NO production in serum by 1.4-fold compared with control. The concentration of l-Arg was significantly higher in ghrelin-treated rats than in control while arginase activity was significantly lower in ghrelin-treated than in control hearts. Ghrelin treatment increased phosphorylation of Akt by 1.9-fold and ERK1/2 by 1.6-fold and increased iNOS expression by 2.5-fold compared with control. In addition, ghrelin treatment increased Nos2 gene expression by 2.2-fold as determined by qRT-PCR. These results indicate that ghrelin regulation of iNOS expression/activity is mediated via Akt/ERK1/2 signaling pathway. These results may be relevant to understanding molecular mechanisms underlying direct cardiovascular actions of ghrelin.
T2  - Journal of Physiology and Biochemistry
T1  - Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats
VL  - 67
IS  - 2
SP  - 195
EP  - 204
DO  - 10.1007/s13105-010-0063-1
ER  - 

@article{
author = "Sudar, Emina and Dobutović, Branislava and Soskić, Sanja S. and Mandušić, Vesna and Žakula, Zorica and Misirkić, Maja and Vucicevic, Ljubica and Janjetović, Kristina D. and Trajković, Vladimir S. and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2011",
abstract = "The purpose of this study was to examine the effects of ghrelin on protein kinase B (Akt) and mitogen-activated protein kinase p42/44 (ERK1/2) activation as well as ghrelin effects on inducible nitric oxide (NO) synthase (iNOS; for gene Nos2) activity/expression in rat hearts. Male Wistar rats were treated with ghrelin (0.3 nmol/5 mu l) or an equal volume of phosphate-buffered saline, injected every 24 h into the lateral cerebral ventricle for 5 days and 2 h after the last treatment the animals were sacrificed. Serum NO, l-arginine (l-Arg), and arginase activity were measured spectrophotometrically. For phosphorylation of Akt, ERK1/2, and iNOS protein expression, Western blot method was used. The expression of Nos2 mRNA was measured by the quantitative real-time polymerase chain reaction (qRT-PCR). Treatment with ghrelin significantly increased NO production in serum by 1.4-fold compared with control. The concentration of l-Arg was significantly higher in ghrelin-treated rats than in control while arginase activity was significantly lower in ghrelin-treated than in control hearts. Ghrelin treatment increased phosphorylation of Akt by 1.9-fold and ERK1/2 by 1.6-fold and increased iNOS expression by 2.5-fold compared with control. In addition, ghrelin treatment increased Nos2 gene expression by 2.2-fold as determined by qRT-PCR. These results indicate that ghrelin regulation of iNOS expression/activity is mediated via Akt/ERK1/2 signaling pathway. These results may be relevant to understanding molecular mechanisms underlying direct cardiovascular actions of ghrelin.",
journal = "Journal of Physiology and Biochemistry",
title = "Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats",
volume = "67",
number = "2",
pages = "195-204",
doi = "10.1007/s13105-010-0063-1"
}

Sudar, E., Dobutović, B., Soskić, S. S., Mandušić, V., Žakula, Z., Misirkić, M., Vucicevic, L., Janjetović, K. D., Trajković, V. S., Mikhailidis, D. P.,& Isenović, E. R.. (2011). Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats. in Journal of Physiology and Biochemistry, 67(2), 195-204.
https://doi.org/10.1007/s13105-010-0063-1

Sudar E, Dobutović B, Soskić SS, Mandušić V, Žakula Z, Misirkić M, Vucicevic L, Janjetović KD, Trajković VS, Mikhailidis DP, Isenović ER. Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats. in Journal of Physiology and Biochemistry. 2011;67(2):195-204.
doi:10.1007/s13105-010-0063-1 .

Sudar, Emina, Dobutović, Branislava, Soskić, Sanja S., Mandušić, Vesna, Žakula, Zorica, Misirkić, Maja, Vucicevic, Ljubica, Janjetović, Kristina D., Trajković, Vladimir S., Mikhailidis, Dimitri P., Isenović, Esma R., "Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats" in Journal of Physiology and Biochemistry, 67, no. 2 (2011):195-204,
https://doi.org/10.1007/s13105-010-0063-1 . .

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 . .

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  - 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  - Bin-Jaliah, Ismaeel
AU  - Ammar, Hania I.
AU  - Mikhailidis, Dimitri P.
AU  - Dallak, Mohammed A.
AU  - Al-Hashem, Fahaid H.
AU  - Haidara, Mohamed A.
AU  - Yassin, Hanaa Z.
AU  - Bahnasi, Abeer A.
AU  - Rashed, Laila A.
AU  - Isenović, Esma R.
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3883
AB  - The role of vascular endothelial growth factor (VEGF) and erythropoietin (EPO) in mediating hypoxic preconditioning under the acute intermittent hypoxic condition (AIH) was investigated in this study. Male Wistar rats were randomly assigned and kept in normoxic conditions, (Nx) or in AIH conditions and subjected to brief cycles hypoxia/reoxygenation. Hearts were isolated, perfused, and subjected to in vitro global ischemia followed by reperfusion. During and at the end of reperfusion, left ventricular developed pressure (LVDP); LV end diastolic pressure (LVEDP); rate pressure product (RPP); peak left ventricular pressure rise (Delta P/Delta t(max)) and heart rate (HR) were measured. Hearts subjected to AIH displayed a significant higher LVDP (P LT .001), RPP (P LT .001), and Delta P/Delta t(max) (P LT .001). Expression of VEGF and EPO were significantly increased at 3, 8, and 24 hours after AIH. Hypoxic training could provide a new approach to enhance endogenous cardioprotective mechanisms.
T2  - Angiology
T1  - Cardiac Adaptive Responses After Hypoxia in an Experimental Model
VL  - 61
IS  - 2
SP  - 145
EP  - 156
DO  - 10.1177/0003319709352486
ER  - 

@article{
author = "Bin-Jaliah, Ismaeel and Ammar, Hania I. and Mikhailidis, Dimitri P. and Dallak, Mohammed A. and Al-Hashem, Fahaid H. and Haidara, Mohamed A. and Yassin, Hanaa Z. and Bahnasi, Abeer A. and Rashed, Laila A. and Isenović, Esma R.",
year = "2010",
abstract = "The role of vascular endothelial growth factor (VEGF) and erythropoietin (EPO) in mediating hypoxic preconditioning under the acute intermittent hypoxic condition (AIH) was investigated in this study. Male Wistar rats were randomly assigned and kept in normoxic conditions, (Nx) or in AIH conditions and subjected to brief cycles hypoxia/reoxygenation. Hearts were isolated, perfused, and subjected to in vitro global ischemia followed by reperfusion. During and at the end of reperfusion, left ventricular developed pressure (LVDP); LV end diastolic pressure (LVEDP); rate pressure product (RPP); peak left ventricular pressure rise (Delta P/Delta t(max)) and heart rate (HR) were measured. Hearts subjected to AIH displayed a significant higher LVDP (P LT .001), RPP (P LT .001), and Delta P/Delta t(max) (P LT .001). Expression of VEGF and EPO were significantly increased at 3, 8, and 24 hours after AIH. Hypoxic training could provide a new approach to enhance endogenous cardioprotective mechanisms.",
journal = "Angiology",
title = "Cardiac Adaptive Responses After Hypoxia in an Experimental Model",
volume = "61",
number = "2",
pages = "145-156",
doi = "10.1177/0003319709352486"
}

Bin-Jaliah, I., Ammar, H. I., Mikhailidis, D. P., Dallak, M. A., Al-Hashem, F. H., Haidara, M. A., Yassin, H. Z., Bahnasi, A. A., Rashed, L. A.,& Isenović, E. R.. (2010). Cardiac Adaptive Responses After Hypoxia in an Experimental Model. in Angiology, 61(2), 145-156.
https://doi.org/10.1177/0003319709352486

Bin-Jaliah I, Ammar HI, Mikhailidis DP, Dallak MA, Al-Hashem FH, Haidara MA, Yassin HZ, Bahnasi AA, Rashed LA, Isenović ER. Cardiac Adaptive Responses After Hypoxia in an Experimental Model. in Angiology. 2010;61(2):145-156.
doi:10.1177/0003319709352486 .

Bin-Jaliah, Ismaeel, Ammar, Hania I., Mikhailidis, Dimitri P., Dallak, Mohammed A., Al-Hashem, Fahaid H., Haidara, Mohamed A., Yassin, Hanaa Z., Bahnasi, Abeer A., Rashed, Laila A., Isenović, Esma R., "Cardiac Adaptive Responses After Hypoxia in an Experimental Model" in Angiology, 61, no. 2 (2010):145-156,
https://doi.org/10.1177/0003319709352486 . .

TY  - JOUR
AU  - Haidara, Mohamed A.
AU  - Yassin, Hanaa Z.
AU  - Žakula, Zorica
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4112
AB  - Numerous studies have shown that increased oxidative stress (OxS) is present in diabetic patients. There is evidence that this OxS can be increased before complications associated with diabetes mellitus (DM) occur. However, the role and influence of OxS in the initiation and progression of DM remains the subject of debate. It has been suggested that in DM, OxS is caused by increased production of reactive oxygen species (ROS), and associated with reduction in antioxidant defenses and altered cellular redox status. Acute and chronic OxS which could enhance the development of complications associated with DM. This review considers recent findings on the role of antioxidants in controlling OxS and the incidence of DM with emphasis on animal and human studies.
T2  - Current Vascular Pharmacology
T1  - Diabetes and Antioxidants: Myth or Reality?
VL  - 8
IS  - 5
SP  - 661
EP  - 672
UR  - https://hdl.handle.net/21.15107/rcub_vinar_4112
ER  - 

@article{
author = "Haidara, Mohamed A. and Yassin, Hanaa Z. and Žakula, Zorica and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2010",
abstract = "Numerous studies have shown that increased oxidative stress (OxS) is present in diabetic patients. There is evidence that this OxS can be increased before complications associated with diabetes mellitus (DM) occur. However, the role and influence of OxS in the initiation and progression of DM remains the subject of debate. It has been suggested that in DM, OxS is caused by increased production of reactive oxygen species (ROS), and associated with reduction in antioxidant defenses and altered cellular redox status. Acute and chronic OxS which could enhance the development of complications associated with DM. This review considers recent findings on the role of antioxidants in controlling OxS and the incidence of DM with emphasis on animal and human studies.",
journal = "Current Vascular Pharmacology",
title = "Diabetes and Antioxidants: Myth or Reality?",
volume = "8",
number = "5",
pages = "661-672",
url = "https://hdl.handle.net/21.15107/rcub_vinar_4112"
}

Haidara, M. A., Yassin, H. Z., Žakula, Z., Mikhailidis, D. P.,& Isenović, E. R.. (2010). Diabetes and Antioxidants: Myth or Reality?. in Current Vascular Pharmacology, 8(5), 661-672.
https://hdl.handle.net/21.15107/rcub_vinar_4112

Haidara MA, Yassin HZ, Žakula Z, Mikhailidis DP, Isenović ER. Diabetes and Antioxidants: Myth or Reality?. in Current Vascular Pharmacology. 2010;8(5):661-672.
https://hdl.handle.net/21.15107/rcub_vinar_4112 .

Haidara, Mohamed A., Yassin, Hanaa Z., Žakula, Zorica, Mikhailidis, Dimitri P., Isenović, Esma R., "Diabetes and Antioxidants: Myth or Reality?" in Current Vascular Pharmacology, 8, no. 5 (2010):661-672,
https://hdl.handle.net/21.15107/rcub_vinar_4112 .

TY  - JOUR
AU  - Haidara, Mohamed A.
AU  - Morsy, Mohamed D.
AU  - Abdel-Razek, Hesham A.
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4145
AB  - Septicemia leads to oxidative stress with overproduction of reactive-oxygen species (ROS) and consumption of endogenous antioxidant enzymes. We tested a twofold hypothesis: (1) does oxidative stress (OxS) induced by sepsis acting alone or in concert with augmented inflammatory processes contributes to sepsis-related vascular dysfunction, and, (2) whether ozone (O(3)) and L-canavanine (CAV) mitigate the negative impact of the aforementioned phenomena. We investigated the relative impact of treatment with CAV and/or O(3) on vascular OxS associated vascular functional changes in septicemic rats. For this study, 60 male Sprague-Dawley rats were used and divided into six experimental groups (n=10): control group (C), sham-operated (Sham), septicemic rats (S), S rats treated with CAV (100 mg/kg. i.p; S+CAV), S rats treated with O(3) (1.2 mg/kg, i.p.; S+O(3)) and S rats treated with both O(3) and CAV (S+O(3)+CAV). After 22 h, the mean arterial blood pressure (MAP), the aortic ring vascular reactivity to phenylephrine, abdominal aortic blood flow (AABF), serum tumor necrosis factor-alpha (TNF-alpha) and plasma nitrite/nitrate (NOx) concentration were measured. In addition, hepatic antioxidant enzyme activities sodium dismutase (SOD) and glutathione peroxidase (GSH-Px) were estimated. Septicemia caused significant elevation of serum TNF-alpha (p LT 0.001) and plasma NOx (p LT 0.001) and significant (p LT 0.001) reduction of AABF (p LT 0.001), aortic vascular response to phenylephrine (p LT 0.001), MAP (p LT 0.001) and hepatic SOD and GSH-Px activity (p LT 0.001) compared with the C group, while treatment with O(3) and/or CAV induced significant amelioration of all those increases. Abnormalities were attenuated to a similar extent with treatment with both O(3) and CAV. These results suggested that concomitant administration of O(3) and CAV alleviated the compromised vascular reactivity in septicemic conditions and prevent its progression into septic shock compared with each alone.
T2  - Journal of Physiology and Biochemistry
T1  - Effects of L-Canavanine and ozone on vascular reactivity in septicemic rats
VL  - 66
IS  - 3
SP  - 255
EP  - 264
DO  - 10.1007/s13105-010-0034-6
ER  - 

@article{
author = "Haidara, Mohamed A. and Morsy, Mohamed D. and Abdel-Razek, Hesham A. and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2010",
abstract = "Septicemia leads to oxidative stress with overproduction of reactive-oxygen species (ROS) and consumption of endogenous antioxidant enzymes. We tested a twofold hypothesis: (1) does oxidative stress (OxS) induced by sepsis acting alone or in concert with augmented inflammatory processes contributes to sepsis-related vascular dysfunction, and, (2) whether ozone (O(3)) and L-canavanine (CAV) mitigate the negative impact of the aforementioned phenomena. We investigated the relative impact of treatment with CAV and/or O(3) on vascular OxS associated vascular functional changes in septicemic rats. For this study, 60 male Sprague-Dawley rats were used and divided into six experimental groups (n=10): control group (C), sham-operated (Sham), septicemic rats (S), S rats treated with CAV (100 mg/kg. i.p; S+CAV), S rats treated with O(3) (1.2 mg/kg, i.p.; S+O(3)) and S rats treated with both O(3) and CAV (S+O(3)+CAV). After 22 h, the mean arterial blood pressure (MAP), the aortic ring vascular reactivity to phenylephrine, abdominal aortic blood flow (AABF), serum tumor necrosis factor-alpha (TNF-alpha) and plasma nitrite/nitrate (NOx) concentration were measured. In addition, hepatic antioxidant enzyme activities sodium dismutase (SOD) and glutathione peroxidase (GSH-Px) were estimated. Septicemia caused significant elevation of serum TNF-alpha (p LT 0.001) and plasma NOx (p LT 0.001) and significant (p LT 0.001) reduction of AABF (p LT 0.001), aortic vascular response to phenylephrine (p LT 0.001), MAP (p LT 0.001) and hepatic SOD and GSH-Px activity (p LT 0.001) compared with the C group, while treatment with O(3) and/or CAV induced significant amelioration of all those increases. Abnormalities were attenuated to a similar extent with treatment with both O(3) and CAV. These results suggested that concomitant administration of O(3) and CAV alleviated the compromised vascular reactivity in septicemic conditions and prevent its progression into septic shock compared with each alone.",
journal = "Journal of Physiology and Biochemistry",
title = "Effects of L-Canavanine and ozone on vascular reactivity in septicemic rats",
volume = "66",
number = "3",
pages = "255-264",
doi = "10.1007/s13105-010-0034-6"
}

Haidara, M. A., Morsy, M. D., Abdel-Razek, H. A., Mikhailidis, D. P.,& Isenović, E. R.. (2010). Effects of L-Canavanine and ozone on vascular reactivity in septicemic rats. in Journal of Physiology and Biochemistry, 66(3), 255-264.
https://doi.org/10.1007/s13105-010-0034-6

Haidara MA, Morsy MD, Abdel-Razek HA, Mikhailidis DP, Isenović ER. Effects of L-Canavanine and ozone on vascular reactivity in septicemic rats. in Journal of Physiology and Biochemistry. 2010;66(3):255-264.
doi:10.1007/s13105-010-0034-6 .

Haidara, Mohamed A., Morsy, Mohamed D., Abdel-Razek, Hesham A., Mikhailidis, Dimitri P., Isenović, Esma R., "Effects of L-Canavanine and ozone on vascular reactivity in septicemic rats" in Journal of Physiology and Biochemistry, 66, no. 3 (2010):255-264,
https://doi.org/10.1007/s13105-010-0034-6 . .