| Role of oxidative-nitrosative stress and downstream pathways in various forms of cardiomyopathy and heart failure. | |
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MedLine Citation:
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PMID: 16026319 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Heart failure is the major cause of hospitalization, morbidity and mortality worldwide. Previous experimental and clinical studies have suggested that there is an increased production of reactive oxygen species (ROS: superoxide, hydrogen peroxide, hydroxyl radical) both in animals and in patients with acute and chronic heart failure. The possible source of increased ROS in the failing myocardium include xanthine and NAD(P)H oxidoreductases, cyclooxygenase, the mitochondrial electron transport chain and activated neutrophils among many others. The excessively produced nitric oxide (NO) derived from NO synthases (NOS) has also been implicated in the pathogenesis of chronic heart failure (CHF). The combination of NO and superoxide yields peroxynitrite, a reactive oxidant, which has been shown to impair cardiac function via multiple mechanisms. Increased oxidative and nitrosative stress also activates the nuclear enzyme poly(ADP-ribose) polymerase (PARP), which importantly contributes to the pathogenesis of cardiac and endothelial dysfunction associated with myocardial infarction, chronic heart failure, diabetes, atherosclerosis, hypertension, aging and various forms of shock. Recent studies have demonstrated that pharmacological inhibition of xanthine oxidase derived superoxide formation, neutralization of peroxynitrite or inhibition of PARP provide significant benefit in various forms of cardiovascular injury. This review discusses the role of oxidative/nitrosative stress and downstream pathways in various forms of cardiomyopathy and heart failure. |
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Authors:
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Zoltan Ungvári; Sachin A Gupte; Fabio A Recchia; Sándor Bátkai; Pál Pacher |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Current vascular pharmacology Volume: 3 ISSN: 1570-1611 ISO Abbreviation: Curr Vasc Pharmacol Publication Date: 2005 Jul |
Date Detail:
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Created Date: 2005-07-19 Completed Date: 2005-08-26 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 101157208 Medline TA: Curr Vasc Pharmacol Country: United Arab Emirates |
Other Details:
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Languages: eng Pagination: 221-9 Citation Subset: IM |
Affiliation:
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Department of Physiology, New York Medical College, Valhalla, 10595, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cardiomyopathies / etiology, metabolism* Cardiomyopathy, Dilated / etiology, metabolism Humans NADPH Oxidase / metabolism Oxidative Stress Poly(ADP-ribose) Polymerases / metabolism* Reactive Nitrogen Species / metabolism* Reactive Oxygen Species / metabolism* Xanthine Oxidase / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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Z01 AA000375-02/AA/NIAAA NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Reactive Nitrogen Species; 0/Reactive Oxygen Species; EC 1.17.3.2/Xanthine Oxidase; EC 1.6.3.1/NADPH Oxidase; EC 2.4.2.30/Poly(ADP-ribose) Polymerases |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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