| TNFα in myocardial ischemia/reperfusion, remodeling and heart failure. | |
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MedLine Citation:
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PMID: 20571888 Owner: NLM Status: In-Process |
Abstract/OtherAbstract:
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TNFα is crucially involved in the pathogenesis and progression of myocardial ischemia/reperfusion injury and heart failure. The formation and release of TNFα and its downstream signal transduction cascade following activation of its two receptor subtypes are characterized. Myocardial TNFα and TNF receptor activation have an ambivalent role in myocardial ischemia/reperfusion injury and protection from it. Excessive TNFα expression and subsequent cardiomyocyte TNF receptor type 1 stimulation induce contractile dysfunction, hypertrophy, fibrosis and cell death, while a lower TNFα concentration and subsequent cardiomyocyte TNF receptor type 2 stimulation are protective. Apart from its concentration and receptor subtype, the myocardial action of TNFα depends on the duration of its exposure and its localization. While detrimental during sustained ischemia, TNFα contributes to ischemic preconditioning protection, no matter whether it is the first, second or third window of protection, and both TNF receptors are involved in the protective signal transduction cascade. Finally, the available clinical attempts to antagonize TNFα in cardiovascular disease, notably heart failure, are critically discussed. |
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Authors:
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Petra Kleinbongard; Rainer Schulz; Gerd Heusch |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Heart failure reviews Volume: 16 ISSN: 1573-7322 ISO Abbreviation: Heart Fail Rev Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2010-12-20 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9612481 Medline TA: Heart Fail Rev Country: United States |
Other Details:
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Languages: eng Pagination: 49-69 Citation Subset: IM |
Affiliation:
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Institut für Pathophysiologie, Universitätsklinikum Essen, Hufelandstrasse 55, 45122, Essen, Germany. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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