Document Detail


Autophagy during cardiac stress: joys and frustrations of autophagy.
MedLine Citation:
PMID:  20148666     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The study of autophagy has been transformed by the cloning of most genes in the pathway and the introduction of GFP-LC3 as a reporter to allow visual assessment of autophagy. The field of cardiac biology is not alone in attempting to understand the implications of autophagy. The purpose of this review is to address some of the controversies and conundrums associated with the evolving studies of autophagy in the heart. Autophagy is a cellular process involving a complex orchestration of regulatory gene products as well as machinery for assembly, selective targeting, and degradation of autophagosomes and their contents. Our understanding of the role of autophagy in human disease is rapidly evolving as investigators examine the process in different tissues and different pathophysiological contexts. In the field of heart disease, autophagy has been examined in the settings of ischemia and reperfusion, preconditioning, cardiac hypertrophy, and heart failure. This review addresses the role of autophagy in cardioprotection, the balance of catabolism and anabolism, the concept of mitochondrial quality control, and the implications of impaired autophagic flux or frustrated autophagy.
Authors:
Roberta A Gottlieb; Robert M Mentzer
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; 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:  2013-06-18    
Medline Journal Info:
Nlm Unique ID:  0370600     Medline TA:  Annu Rev Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  45-59     Citation Subset:  IM    
Affiliation:
The BioScience Center, San Diego State University, San Diego, CA 92182, USA. robbieg@sciences.sdsu.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Autophagy / physiology*
Heart / physiology*
Heart Diseases / pathology*
Humans
Insulin / physiology
Mitochondria, Heart / pathology,  physiology
Myocardial Ischemia / pathology
Signal Transduction / physiology
Stress, Physiological*
Grant Support
ID/Acronym/Agency:
P01 HL085577/HL/NHLBI NIH HHS; P01 HL85577/HL/NHLBI NIH HHS; R01 AG033283/AG/NIA NIH HHS; R01 AG33283/AG/NIA NIH HHS; R01 HL034579/HL/NHLBI NIH HHS; R01 HL34579/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Insulin
Comments/Corrections

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