TY  - JOUR
AU  - Abate, Nicola
AU  - Sallam, Hanaa S.
AU  - Rizzo, Manfredi
AU  - Nikolić, Dragana
AU  - Obradović, Milan M.
AU  - Bjelogrlic, Predrag
AU  - Isenović, Esma R.
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/56
AB  - Resistin is an adipocyte-and monocyte-derived cytokine which has been implicated in the modulation of insulin action, energy, glucose and lipid homeostasis. Resistin has been associated with insulin resistance and many of its known complications. As a molecular link between metabolic signals, inflammation, and vascular dysfunction, resistin can be proposed as playing a significant role in the heightened inflammatory state induced by metabolic stress linked to excessive caloric intake, thus contributing to the risk for metabolic syndrome (MetS), type 2 diabetes (T2DM), and cardiovascular diseases (CVD). In this review, we highlighted the role of resistin, as an inflammatory cytokine, in the development of CVD, T2DM and the MetS.
T2  - Current Pharmaceutical Design
T1  - Resistin: An Inflammatory Cytokine. Role in Cardiovascular Diseases, Diabetes and the Metabolic Syndrome
VL  - 20
IS  - 31
SP  - 4961
EP  - 4969
UR  - https://hdl.handle.net/21.15107/rcub_vinar_56
ER  - 

@article{
author = "Abate, Nicola and Sallam, Hanaa S. and Rizzo, Manfredi and Nikolić, Dragana and Obradović, Milan M. and Bjelogrlic, Predrag and Isenović, Esma R.",
year = "2014",
abstract = "Resistin is an adipocyte-and monocyte-derived cytokine which has been implicated in the modulation of insulin action, energy, glucose and lipid homeostasis. Resistin has been associated with insulin resistance and many of its known complications. As a molecular link between metabolic signals, inflammation, and vascular dysfunction, resistin can be proposed as playing a significant role in the heightened inflammatory state induced by metabolic stress linked to excessive caloric intake, thus contributing to the risk for metabolic syndrome (MetS), type 2 diabetes (T2DM), and cardiovascular diseases (CVD). In this review, we highlighted the role of resistin, as an inflammatory cytokine, in the development of CVD, T2DM and the MetS.",
journal = "Current Pharmaceutical Design",
title = "Resistin: An Inflammatory Cytokine. Role in Cardiovascular Diseases, Diabetes and the Metabolic Syndrome",
volume = "20",
number = "31",
pages = "4961-4969",
url = "https://hdl.handle.net/21.15107/rcub_vinar_56"
}

Abate, N., Sallam, H. S., Rizzo, M., Nikolić, D., Obradović, M. M., Bjelogrlic, P.,& Isenović, E. R.. (2014). Resistin: An Inflammatory Cytokine. Role in Cardiovascular Diseases, Diabetes and the Metabolic Syndrome. in Current Pharmaceutical Design, 20(31), 4961-4969.
https://hdl.handle.net/21.15107/rcub_vinar_56

Abate N, Sallam HS, Rizzo M, Nikolić D, Obradović MM, Bjelogrlic P, Isenović ER. Resistin: An Inflammatory Cytokine. Role in Cardiovascular Diseases, Diabetes and the Metabolic Syndrome. in Current Pharmaceutical Design. 2014;20(31):4961-4969.
https://hdl.handle.net/21.15107/rcub_vinar_56 .

Abate, Nicola, Sallam, Hanaa S., Rizzo, Manfredi, Nikolić, Dragana, Obradović, Milan M., Bjelogrlic, Predrag, Isenović, Esma R., "Resistin: An Inflammatory Cytokine. Role in Cardiovascular Diseases, Diabetes and the Metabolic Syndrome" in Current Pharmaceutical Design, 20, no. 31 (2014):4961-4969,
https://hdl.handle.net/21.15107/rcub_vinar_56 .

TY  - JOUR
AU  - Kypreos, Kyriakos E.
AU  - Zafirović, Sonja
AU  - Petropoulou, Peristera-Ioanna
AU  - Bjelogrlic, Predrag
AU  - Resanović, Ivana
AU  - Traish, Abdul
AU  - Isenović, Esma R.
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5954
AB  - Estrogens have been recognized, in the last 3 decades, as important hormones in direct and indirect modulation of vascular health. In addition to their direct benefit on cardiovascular health, the presence of esterified estrogen in the lipid core of high-density lipoprotein (HDL) particles indirectly contributes to atheroprotection by significantly improving HDL quality and functionality. Estrogens modulate their physiological activity via genomic and nongenomic mechanisms. Genomic mechanisms are thought to be mediated directly by interaction of the hormone receptor complex with the hormone response elements that regulate gene expression. Nongenomic mechanisms are thought to occur via interaction of the estrogen with membrane-bound receptors, which rapidly activate intracellular signaling without binding of the hormone receptor complex to its hormone response elements. Estradiol in particular mediates early and late endothelial nitric oxide synthase (eNOS) activation via interaction with estrogen receptors through both nongenomic and genomic mechanisms. In the vascular system, the primary endogenous source of nitric oxide (NO) generation is eNOS. Nitric oxide primarily influences blood vessel relaxation, the heart rate, and myocyte contractility. The abnormalities in expression and/or functions of eNOS lead to the development of cardiovascular diseases, both in animals and in humans. Although considerable research efforts have been dedicated to understanding the mechanisms of action of estradiol in regulating cardiac eNOS, more research is needed to fully understand the details of such mechanisms. This review focuses on recent findings from animal and human studies on the regulation of eNOS and HDL quality by estradiol in cardiovascular pathology.
T2  - Journal of Cardiovascular Pharmacology and Therapeutics
T1  - Regulation of Endothelial Nitric Oxide Synthase and High-Density Lipoprotein Quality by Estradiol in Cardiovascular Pathology
VL  - 19
IS  - 3
SP  - 256
EP  - 268
DO  - 10.1177/1074248413513499
ER  - 

@article{
author = "Kypreos, Kyriakos E. and Zafirović, Sonja and Petropoulou, Peristera-Ioanna and Bjelogrlic, Predrag and Resanović, Ivana and Traish, Abdul and Isenović, Esma R.",
year = "2014",
abstract = "Estrogens have been recognized, in the last 3 decades, as important hormones in direct and indirect modulation of vascular health. In addition to their direct benefit on cardiovascular health, the presence of esterified estrogen in the lipid core of high-density lipoprotein (HDL) particles indirectly contributes to atheroprotection by significantly improving HDL quality and functionality. Estrogens modulate their physiological activity via genomic and nongenomic mechanisms. Genomic mechanisms are thought to be mediated directly by interaction of the hormone receptor complex with the hormone response elements that regulate gene expression. Nongenomic mechanisms are thought to occur via interaction of the estrogen with membrane-bound receptors, which rapidly activate intracellular signaling without binding of the hormone receptor complex to its hormone response elements. Estradiol in particular mediates early and late endothelial nitric oxide synthase (eNOS) activation via interaction with estrogen receptors through both nongenomic and genomic mechanisms. In the vascular system, the primary endogenous source of nitric oxide (NO) generation is eNOS. Nitric oxide primarily influences blood vessel relaxation, the heart rate, and myocyte contractility. The abnormalities in expression and/or functions of eNOS lead to the development of cardiovascular diseases, both in animals and in humans. Although considerable research efforts have been dedicated to understanding the mechanisms of action of estradiol in regulating cardiac eNOS, more research is needed to fully understand the details of such mechanisms. This review focuses on recent findings from animal and human studies on the regulation of eNOS and HDL quality by estradiol in cardiovascular pathology.",
journal = "Journal of Cardiovascular Pharmacology and Therapeutics",
title = "Regulation of Endothelial Nitric Oxide Synthase and High-Density Lipoprotein Quality by Estradiol in Cardiovascular Pathology",
volume = "19",
number = "3",
pages = "256-268",
doi = "10.1177/1074248413513499"
}

Kypreos, K. E., Zafirović, S., Petropoulou, P., Bjelogrlic, P., Resanović, I., Traish, A.,& Isenović, E. R.. (2014). Regulation of Endothelial Nitric Oxide Synthase and High-Density Lipoprotein Quality by Estradiol in Cardiovascular Pathology. in Journal of Cardiovascular Pharmacology and Therapeutics, 19(3), 256-268.
https://doi.org/10.1177/1074248413513499

Kypreos KE, Zafirović S, Petropoulou P, Bjelogrlic P, Resanović I, Traish A, Isenović ER. Regulation of Endothelial Nitric Oxide Synthase and High-Density Lipoprotein Quality by Estradiol in Cardiovascular Pathology. in Journal of Cardiovascular Pharmacology and Therapeutics. 2014;19(3):256-268.
doi:10.1177/1074248413513499 .

Kypreos, Kyriakos E., Zafirović, Sonja, Petropoulou, Peristera-Ioanna, Bjelogrlic, Predrag, Resanović, Ivana, Traish, Abdul, Isenović, Esma R., "Regulation of Endothelial Nitric Oxide Synthase and High-Density Lipoprotein Quality by Estradiol in Cardiovascular Pathology" in Journal of Cardiovascular Pharmacology and Therapeutics, 19, no. 3 (2014):256-268,
https://doi.org/10.1177/1074248413513499 . .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Bjelogrlic, Predrag
AU  - Rizzo, Manfredi
AU  - Katsiki, Niki
AU  - Haidara, Mohamed A.
AU  - Stewart, Alan J.
AU  - Jovanović, Aleksandra
AU  - Isenović, Esma R.
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5672
AB  - Obesity is associated with aberrant sodium/potassium-ATPase (Na+/K+-ATPase) activity, apparently linked to hyperglycemic hyperinsulinemia, which may repress or inactivate the enzyme. The reduction of Na+/K+-ATPase activity in cardiac tissue induces myocyte death and cardiac dysfunction, leading to the development of myocardial dilation in animal models; this has also been documented in patients with heart failure (HF). During several pathological situations (cardiac insufficiency and HF) and in experimental models (obesity), the heart becomes more sensitive to the effect of cardiac glycosides, due to a decrease in Na+/K+-ATPase levels. The primary female sex steroid estradiol has long been recognized to be important in a wide variety of physiological processes. Numerous studies, including ours, have shown that estradiol is one of the major factors controlling the activity and expression of Na+/K+-ATPase in the cardiovascular (CV) system. However, the effects of estradiol on Na+/K+-ATPase in both normal and pathological conditions, such as obesity, remain unclear. Increasing our understanding of the molecular mechanisms by which estradiol mediates its effects on Na+/K+-ATPase function may help to develop new strategies for the treatment of CV diseases. Herein, we discuss the latest data from animal and clinical studies that have examined how pathophysiological conditions such as obesity and the action of estradiol regulate Na+/K+-ATPase activity.
T2  - Journal of Endocrinology
T1  - Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases
VL  - 218
IS  - 3
SP  - R13
EP  - R23
DO  - 10.1530/JOE-13-0144
ER  - 

@article{
author = "Obradović, Milan M. and Bjelogrlic, Predrag and Rizzo, Manfredi and Katsiki, Niki and Haidara, Mohamed A. and Stewart, Alan J. and Jovanović, Aleksandra and Isenović, Esma R.",
year = "2013",
abstract = "Obesity is associated with aberrant sodium/potassium-ATPase (Na+/K+-ATPase) activity, apparently linked to hyperglycemic hyperinsulinemia, which may repress or inactivate the enzyme. The reduction of Na+/K+-ATPase activity in cardiac tissue induces myocyte death and cardiac dysfunction, leading to the development of myocardial dilation in animal models; this has also been documented in patients with heart failure (HF). During several pathological situations (cardiac insufficiency and HF) and in experimental models (obesity), the heart becomes more sensitive to the effect of cardiac glycosides, due to a decrease in Na+/K+-ATPase levels. The primary female sex steroid estradiol has long been recognized to be important in a wide variety of physiological processes. Numerous studies, including ours, have shown that estradiol is one of the major factors controlling the activity and expression of Na+/K+-ATPase in the cardiovascular (CV) system. However, the effects of estradiol on Na+/K+-ATPase in both normal and pathological conditions, such as obesity, remain unclear. Increasing our understanding of the molecular mechanisms by which estradiol mediates its effects on Na+/K+-ATPase function may help to develop new strategies for the treatment of CV diseases. Herein, we discuss the latest data from animal and clinical studies that have examined how pathophysiological conditions such as obesity and the action of estradiol regulate Na+/K+-ATPase activity.",
journal = "Journal of Endocrinology",
title = "Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases",
volume = "218",
number = "3",
pages = "R13-R23",
doi = "10.1530/JOE-13-0144"
}

Obradović, M. M., Bjelogrlic, P., Rizzo, M., Katsiki, N., Haidara, M. A., Stewart, A. J., Jovanović, A.,& Isenović, E. R.. (2013). Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases. in Journal of Endocrinology, 218(3), R13-R23.
https://doi.org/10.1530/JOE-13-0144

Obradović MM, Bjelogrlic P, Rizzo M, Katsiki N, Haidara MA, Stewart AJ, Jovanović A, Isenović ER. Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases. in Journal of Endocrinology. 2013;218(3):R13-R23.
doi:10.1530/JOE-13-0144 .

Obradović, Milan M., Bjelogrlic, Predrag, Rizzo, Manfredi, Katsiki, Niki, Haidara, Mohamed A., Stewart, Alan J., Jovanović, Aleksandra, Isenović, Esma R., "Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases" in Journal of Endocrinology, 218, no. 3 (2013):R13-R23,
https://doi.org/10.1530/JOE-13-0144 . .