Document Detail


Impaired myocardial autophagy linked to energy metabolism disorders.
MedLine Citation:
PMID:  22722538     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Autophagy represents an evolutionarily conserved catabolic mechanism that promotes cell survival by releasing energy substrates via degradation of cellular constituents and by eliminating defective organelles under conditions of stress, such as starvation and hypoxia. The link between enhanced autophagy and nutrient deprivation has been well established. For example, chronic myocardial ischemia, a condition of insufficient oxygen and nutrition, activates autophagy to degrade and recycle damaged cellular structures, thereby ameliorating cardiomyocyte injury.
Authors:
Zi-Lun Li; Lilach O Lerman
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-06-01
Journal Detail:
Title:  Autophagy     Volume:  8     ISSN:  1554-8635     ISO Abbreviation:  Autophagy     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-08-24     Completed Date:  2013-01-03     Revised Date:  2013-06-03    
Medline Journal Info:
Nlm Unique ID:  101265188     Medline TA:  Autophagy     Country:  United States    
Other Details:
Languages:  eng     Pagination:  992-4     Citation Subset:  IM    
Affiliation:
Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.
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MeSH Terms
Descriptor/Qualifier:
Autophagy*
Energy Metabolism*
Humans
Insulin Resistance
Metabolic Syndrome X / pathology*
Models, Biological
Myocardium / pathology*
Sirtuin 1 / metabolism
Grant Support
ID/Acronym/Agency:
DK73608/DK/NIDDK NIH HHS; HL085307/HL/NHLBI NIH HHS; HL77131/HL/NHLBI NIH HHS; R01 DK073608/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
EC 3.5.1.-/Sirtuin 1

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


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