Document Detail


Cell death in the pathogenesis of heart disease: mechanisms and significance.
MedLine Citation:
PMID:  20148665     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cell death was once viewed as unregulated. It is now clear that at least a portion of cell death is a regulated cell suicide process. This type of death can exhibit multiple morphologies. One of these, apoptosis, has long been recognized to be actively mediated, and many of its underlying mechanisms have been elucidated. Moreover, necrosis, the traditional example of unregulated cell death, is also regulated in some instances. Autophagy is usually a survival mechanism but can occur in association with cell death. Little is known, however, about how autophagic cells die. Apoptosis, necrosis, and autophagy occur in cardiac myocytes during myocardial infarction, ischemia/reperfusion, and heart failure. Pharmacological and genetic inhibition of apoptosis and necrosis lessens infarct size and improves cardiac function in these disorders. The roles of autophagy in ischemia/reperfusion and heart failure are unresolved. A better understanding of these processes and their interrelationships may allow for the development of novel therapies for the major heart syndromes.
Authors:
Russell S Whelan; Vladimir Kaplinskiy; Richard N Kitsis
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Annual review of physiology     Volume:  72     ISSN:  1545-1585     ISO Abbreviation:  Annu. Rev. Physiol.     Publication Date:  2010  
Date Detail:
Created Date:  2010-02-12     Completed Date:  2010-05-04     Revised Date:  2012-03-22    
Medline Journal Info:
Nlm Unique ID:  0370600     Medline TA:  Annu Rev Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  19-44     Citation Subset:  IM    
Affiliation:
Wilf Family Cardiovascular Research Institute and the Departments of Medicine and Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / drug effects,  physiology
Autophagy / drug effects,  physiology
Cell Death / drug effects,  physiology*
Heart Diseases / drug therapy,  pathology*
Heart Failure / pathology
Humans
Mitochondria, Heart / physiology
Myocardial Infarction / pathology
Necrosis / pathology
Signal Transduction / drug effects,  physiology
Grant Support
ID/Acronym/Agency:
P01HL078825/HL/NHLBI NIH HHS; P60DK020541/DK/NIDDK NIH HHS; R01HL60665/HL/NHLBI NIH HHS

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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