Document Detail


Cardiac autophagy: good with the bad.
MedLine Citation:
PMID:  22743635     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Stress-induced hypertrophic growth of the myocardium is a pathogenetic milestone in the progression of heart failure. Some evidence suggests that suppression of pathological cardiac hypertrophy per se is a viable target for therapeutic intervention, and cardiomyocyte autophagy is an attractive mechanism for consideration as a means of controlling the hypertrophic response. However, although considerable insights have been gleaned in the molecular mechanisms governing cardiomyocyte autophagy, many details critical to rational targeting of the response remain unknown. Among them, mechanisms underlying the adaptive and maladaptive features of autophagy are obscure. With time and further study, it is possible that this near-ubiquitous cardiac response to stress will emerge as a target for therapeutic manipulation.
Authors:
Oktay F Rifki; Joseph A Hill
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Journal of cardiovascular pharmacology     Volume:  60     ISSN:  1533-4023     ISO Abbreviation:  J. Cardiovasc. Pharmacol.     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-09-11     Completed Date:  2013-07-09     Revised Date:  2013-09-03    
Medline Journal Info:
Nlm Unique ID:  7902492     Medline TA:  J Cardiovasc Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  248-52     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine (Cardiology), University of Texas Southwestern Medical Center, Dallas, TX, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Autophagy / drug effects,  physiology*
Cardiomegaly / drug therapy,  pathology*,  physiopathology*
Heart / drug effects,  physiology
Histone Deacetylase Inhibitors / pharmacology,  therapeutic use
Humans
Myocardium / pathology
Myocytes, Cardiac / drug effects,  pathology,  physiology
Grant Support
ID/Acronym/Agency:
HL-075173/HL/NHLBI NIH HHS; HL-080144/HL/NHLBI NIH HHS; HL-090842/HL/NHLBI NIH HHS; P30 HL101254/HL/NHLBI NIH HHS; R01 HL075173/HL/NHLBI NIH HHS; R01 HL080144/HL/NHLBI NIH HHS; R01 HL090842/HL/NHLBI NIH HHS; U01 HL100401/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Histone Deacetylase Inhibitors
Comments/Corrections

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


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