Document Detail

Molecular mechanisms and physiological significance of autophagy during myocardial ischemia and reperfusion.
MedLine Citation:
PMID:  18227645     Owner:  NLM     Status:  MEDLINE    
Autophagy is an intracellular bulk degradation process whereby cytoplasmic proteins and organelles are degraded and recycled through lysosomes. In the heart, autophagy plays a homeostatic role at basal levels, and the absence of autophagy causes cardiac dysfunction and the development of cardiomyopathy. Autophagy is induced during myocardial ischemia and further enhanced by reperfusion. Although induction of autophagy during the ischemic phase is protective, further enhancement of autophagy during the reperfusion phase may induce cell death and appears to be detrimental. In this review we discuss the functional significance of autophagy and the underlying signaling mechanism in the heart during ischemia/reperfusion.
Yutaka Matsui; Shiori Kyoi; Hiromitsu Takagi; Chiao-Po Hsu; Nirmala Hariharan; Tetsuro Ago; Stephen F Vatner; Junichi Sadoshima
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2008-01-24
Journal Detail:
Title:  Autophagy     Volume:  4     ISSN:  1554-8635     ISO Abbreviation:  Autophagy     Publication Date:  2008 May 
Date Detail:
Created Date:  2008-04-25     Completed Date:  2008-09-04     Revised Date:  2013-06-06    
Medline Journal Info:
Nlm Unique ID:  101265188     Medline TA:  Autophagy     Country:  United States    
Other Details:
Languages:  eng     Pagination:  409-15     Citation Subset:  IM    
Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, New Jersey 07103, USA.
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MeSH Terms
AMP-Activated Protein Kinases
Autophagy / physiology*
Cell Survival
Hypoxia-Inducible Factor 1 / metabolism
Multienzyme Complexes / metabolism
Myocardial Ischemia*
Myocardial Reperfusion*
Protein-Serine-Threonine Kinases / metabolism
Signal Transduction / physiology
Grant Support
HL59139/HL/NHLBI NIH HHS; HL67724/HL/NHLBI NIH HHS; HL67727/HL/NHLBI NIH HHS; HL69020/HL/NHLBI NIH HHS; HL73048/HL/NHLBI NIH HHS; P01 HL059139-060011/HL/NHLBI NIH HHS; P01 HL059139-10/HL/NHLBI NIH HHS; P01 HL069020-060007/HL/NHLBI NIH HHS; P01 HL069020-070007/HL/NHLBI NIH HHS; P01 HL069020-080007/HL/NHLBI NIH HHS; R01 HL033107-27/HL/NHLBI NIH HHS; R01 HL067724-06/HL/NHLBI NIH HHS; R01 HL067724-07/HL/NHLBI NIH HHS; R01 HL067724-08/HL/NHLBI NIH HHS; R01 HL067724-09/HL/NHLBI NIH HHS; R01 HL067727-01/HL/NHLBI NIH HHS
Reg. No./Substance:
0/Hypoxia-Inducible Factor 1; 0/Multienzyme Complexes; EC Protein Kinases; EC Kinases

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

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