Document Detail


Acute induction of autophagy as a novel strategy for cardioprotection: getting to the heart of the matter.
MedLine Citation:
PMID:  21187719     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
There is no question that necrosis and apoptosis contribute to cardiomyocyte death in the setting of myocardial ischemia-reperfusion. Indeed, considerable effort and resources have been invested in the development of novel therapies aimed at attenuating necrotic and apoptotic cell death, with the ultimate goal of applying these strategies to reduce infarct size and improve outcome in patients suffering acute myocardial infarction (MI) or 'heart attack'. However, an issue that remains controversial is the role of autophagy in determining the fate of ischemic-reperfused cardiomyocytes: i.e., is induction of autophagy detrimental or protective? Recent data from our group obtained in the clinically relevant, in vivo swine model of acute MI provides novel evidence of a positive association between pharmacological upregulation of autophagy (achieved by administration of chloramphenicol succinate (CAPS)) and increased resistance to myocardial ischemia-reperfusion injury.
Authors:
Karin Przyklenk; Vishnu Vardhan Reddy Undyala; Joseph Wider; Javier A Sala-Mercado; Roberta A Gottlieb; Robert M Mentzer
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Publication Detail:
Type:  Journal Article     Date:  2011-04-01
Journal Detail:
Title:  Autophagy     Volume:  7     ISSN:  1554-8635     ISO Abbreviation:  Autophagy     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-06-30     Completed Date:  2011-09-19     Revised Date:  2013-06-17    
Medline Journal Info:
Nlm Unique ID:  101265188     Medline TA:  Autophagy     Country:  United States    
Other Details:
Languages:  eng     Pagination:  432-3     Citation Subset:  IM    
Affiliation:
Cardiovascular Research Institute, Wayne State University, Detroit, MI, USA. kprzykle@med.wayne.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis
Autophagy*
Chloramphenicol / analogs & derivatives,  pharmacology
Disease Models, Animal
Models, Biological
Myocardial Reperfusion Injury / pathology
Myocardium / metabolism
Myocytes, Cardiac / cytology*
Necrosis / metabolism
Phenotype
Phosphatidylinositol 3-Kinases / metabolism
Signal Transduction
Swine
Time Factors
Grant Support
ID/Acronym/Agency:
R01 HL060590/HL/NHLBI NIH HHS; R01 HL071091/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
56-75-7/Chloramphenicol; EC 2.7.1.-/Phosphatidylinositol 3-Kinases; ZCX619U9A1/chloramphenicol succinate

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


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