Document Detail

Autophagy in the stress-induced myocardium.
MedLine Citation:
PMID:  22202025     Owner:  NLM     Status:  In-Data-Review    
Cardiovascular disease is a leading cause of death worldwide, particularly in Western societies. During an ischaemic insult, ventricular pressure from the heart is diminished as a result of cardiac myocyte death by necrosis and apoptosis. Autophagy is a process whereby cells catabolise intracellular proteins in order to generate ATP in times of stress such as nutrient starvation and hypoxia. Emerging evidence suggests that autophagy plays a positive role in cardiac myocyte survival during periods of cellular stress performing an important damage limitation function. By promoting cell survival, cardiac myocyte loss is reduced thereby minimising the potential of heart failure. In contrast, it has been reported that autophagy can also be a form of cell death. By considering the various animal models of autophagy, we examine the role of the Signal Transducers and Activator of Transcription (STAT) proteins in the autophagic response. Additionally we review the role of the tumour suppressor, p53 and its family member p73 and their potential role in the autophagic response.
James McCormick; Richard A Knight; Sean P Barry; Tiziano M Scarabelli; Kadija Abounit; David S Latchman; Anastasis Stephanou
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Publication Detail:
Type:  Journal Article     Date:  2012-01-01
Journal Detail:
Title:  Frontiers in bioscience (Elite edition)     Volume:  4     ISSN:  1945-0508     ISO Abbreviation:  Front Biosci (Elite Ed)     Publication Date:  2012  
Date Detail:
Created Date:  2011-12-28     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101485240     Medline TA:  Front Biosci (Elite Ed)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2131-41     Citation Subset:  IM    
The Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH.
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