TY  - CHAP
AU  - Sudar, Emina
AU  - Soskić, Sanja
AU  - Zarić, Božidarka L.
AU  - Rašić-Milutinović, Zorica
AU  - Smiljanić, Katarina
AU  - Radak, Đorđe
AU  - Mikhailidis, Dimitri
AU  - Rizzo, Manfredi
AU  - Isenović, Esma
PY  - 2012
UR  - https://cherry.chem.bg.ac.rs/handle/123456789/3919
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.
PB  - Nova Science Publishers Inc, New York
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_cherry_3919
ER  - 

@inbook{
author = "Sudar, Emina and Soskić, Sanja and Zarić, Božidarka L. and Rašić-Milutinović, Zorica and Smiljanić, Katarina and Radak, Đorđe and Mikhailidis, Dimitri and Rizzo, Manfredi and Isenović, Esma",
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.",
publisher = "Nova Science Publishers Inc, New York",
journal = "Ghrelin: Production, Action Mechanisms and Physiological Effects",
booktitle = "Ghrelin, obesity and atherosclerosis",
pages = "111-126",
url = "https://hdl.handle.net/21.15107/rcub_cherry_3919"
}

Sudar, E., Soskić, S., Zarić, B. L., Rašić-Milutinović, Z., Smiljanić, K., Radak, Đ., Mikhailidis, D., Rizzo, M.,& Isenović, E.. (2012). Ghrelin, obesity and atherosclerosis. in Ghrelin: Production, Action Mechanisms and Physiological Effects
Nova Science Publishers Inc, New York., 111-126.
https://hdl.handle.net/21.15107/rcub_cherry_3919

Sudar E, Soskić S, Zarić BL, Rašić-Milutinović Z, Smiljanić K, Radak Đ, Mikhailidis D, Rizzo M, Isenović E. Ghrelin, obesity and atherosclerosis. in Ghrelin: Production, Action Mechanisms and Physiological Effects. 2012;:111-126.
https://hdl.handle.net/21.15107/rcub_cherry_3919 .

Sudar, Emina, Soskić, Sanja, Zarić, Božidarka L., Rašić-Milutinović, Zorica, Smiljanić, Katarina, Radak, Đorđe, Mikhailidis, Dimitri, Rizzo, Manfredi, Isenović, Esma, "Ghrelin, obesity and atherosclerosis" in Ghrelin: Production, Action Mechanisms and Physiological Effects (2012):111-126,
https://hdl.handle.net/21.15107/rcub_cherry_3919 .

TY  - CHAP
AU  - Sudar, Emina
AU  - Soskić, Sanja
AU  - Zarić, Božidarka L.
AU  - Rašić-Milutinović, Zorica
AU  - Smiljanić, Katarina
AU  - Radak, Đorđe
AU  - Mikhailidis, Dimitri
AU  - Rizzo, Manfredi
AU  - Isenović, Esma
PY  - 2012
UR  - https://cherry.chem.bg.ac.rs/handle/123456789/3920
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.
PB  - Nova Science Publishers Inc, New York
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_cherry_3920
ER  - 

@inbook{
author = "Sudar, Emina and Soskić, Sanja and Zarić, Božidarka L. and Rašić-Milutinović, Zorica and Smiljanić, Katarina and Radak, Đorđe and Mikhailidis, Dimitri and Rizzo, Manfredi and Isenović, Esma",
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.",
publisher = "Nova Science Publishers Inc, New York",
journal = "Ghrelin: Production, Action Mechanisms and Physiological Effects",
booktitle = "Ghrelin, obesity and atherosclerosis",
pages = "111-126",
url = "https://hdl.handle.net/21.15107/rcub_cherry_3920"
}

Sudar, E., Soskić, S., Zarić, B. L., Rašić-Milutinović, Z., Smiljanić, K., Radak, Đ., Mikhailidis, D., Rizzo, M.,& Isenović, E.. (2012). Ghrelin, obesity and atherosclerosis. in Ghrelin: Production, Action Mechanisms and Physiological Effects
Nova Science Publishers Inc, New York., 111-126.
https://hdl.handle.net/21.15107/rcub_cherry_3920

Sudar E, Soskić S, Zarić BL, Rašić-Milutinović Z, Smiljanić K, Radak Đ, Mikhailidis D, Rizzo M, Isenović E. Ghrelin, obesity and atherosclerosis. in Ghrelin: Production, Action Mechanisms and Physiological Effects. 2012;:111-126.
https://hdl.handle.net/21.15107/rcub_cherry_3920 .

Sudar, Emina, Soskić, Sanja, Zarić, Božidarka L., Rašić-Milutinović, Zorica, Smiljanić, Katarina, Radak, Đorđe, Mikhailidis, Dimitri, Rizzo, Manfredi, Isenović, Esma, "Ghrelin, obesity and atherosclerosis" in Ghrelin: Production, Action Mechanisms and Physiological Effects (2012):111-126,
https://hdl.handle.net/21.15107/rcub_cherry_3920 .

TY  - JOUR
AU  - Dobutović, Branislava
AU  - Smiljanić, Katarina
AU  - Soskić, Sanja
AU  - Dungen, Hans-Dirk
AU  - Isenović, Esma
PY  - 2011
UR  - https://cherry.chem.bg.ac.rs/handle/123456789/3918
AB  - Nitric oxide synthases (NOS) are the enzymes responsible for nitric oxide (NO) generation. NO is a free radical which reacts with various molecules to cause multiple biological effects. It is clear that the generation and actions of NO under physiological and pathophysiological conditions are exquisitely regulated and extend to almost every cell type and function within the circulation. While the molecule mediates many physiological functions, an excessive presence of NO is toxic to cells. The enzyme NOS, constitutively or inductively, catalyses the production of NO in several biological systems. NO is derived not only from NOS isoforms but also from NOS-independent sources. In mammals, to date, three distinct NOS isoforms have been identified: neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). The molecular structure, enzymology and pharmacology of these enzymes have been well defined, and reveal critical roles for the NOS system in a variety of important physiological processes. This review focuses on recent advances in the understanding of the interactions between NOS enzymes and pathophysiology of cardiovascular diseases (CVD) and the role of NO agonists as potential therapeutic agents in treatment of CVD.
PB  - Bentham Open
T2  - The Open Nitric Oxide Journal
T1  - Nitric Oxide and its Role in Cardiovascular Diseases
VL  - 3
IS  - 1
SP  - 65
EP  - 71
DO  - 10.2174/1875042701103010065
ER  - 

@article{
author = "Dobutović, Branislava and Smiljanić, Katarina and Soskić, Sanja and Dungen, Hans-Dirk and Isenović, Esma",
year = "2011",
abstract = "Nitric oxide synthases (NOS) are the enzymes responsible for nitric oxide (NO) generation. NO is a free radical which reacts with various molecules to cause multiple biological effects. It is clear that the generation and actions of NO under physiological and pathophysiological conditions are exquisitely regulated and extend to almost every cell type and function within the circulation. While the molecule mediates many physiological functions, an excessive presence of NO is toxic to cells. The enzyme NOS, constitutively or inductively, catalyses the production of NO in several biological systems. NO is derived not only from NOS isoforms but also from NOS-independent sources. In mammals, to date, three distinct NOS isoforms have been identified: neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). The molecular structure, enzymology and pharmacology of these enzymes have been well defined, and reveal critical roles for the NOS system in a variety of important physiological processes. This review focuses on recent advances in the understanding of the interactions between NOS enzymes and pathophysiology of cardiovascular diseases (CVD) and the role of NO agonists as potential therapeutic agents in treatment of CVD.",
publisher = "Bentham Open",
journal = "The Open Nitric Oxide Journal",
title = "Nitric Oxide and its Role in Cardiovascular Diseases",
volume = "3",
number = "1",
pages = "65-71",
doi = "10.2174/1875042701103010065"
}

Dobutović, B., Smiljanić, K., Soskić, S., Dungen, H.,& Isenović, E.. (2011). Nitric Oxide and its Role in Cardiovascular Diseases. in The Open Nitric Oxide Journal
Bentham Open., 3(1), 65-71.
https://doi.org/10.2174/1875042701103010065

Dobutović B, Smiljanić K, Soskić S, Dungen H, Isenović E. Nitric Oxide and its Role in Cardiovascular Diseases. in The Open Nitric Oxide Journal. 2011;3(1):65-71.
doi:10.2174/1875042701103010065 .

Dobutović, Branislava, Smiljanić, Katarina, Soskić, Sanja, Dungen, Hans-Dirk, Isenović, Esma, "Nitric Oxide and its Role in Cardiovascular Diseases" in The Open Nitric Oxide Journal, 3, no. 1 (2011):65-71,
https://doi.org/10.2174/1875042701103010065 . .