Document Detail


Autophagy in hypertensive heart disease.
MedLine Citation:
PMID:  20118246     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In response to hypertension, the heart manifests robust hypertrophic growth, which offsets load-induced elevations in wall stress. If sustained, this hypertrophic response is a major risk factor for systolic dysfunction and heart failure. Extensive research efforts have focused on the progression from hypertrophy to failure; however, precise understanding of underlying mechanisms remains elusive. Recently, autophagy, a process of cellular cannibalization, has been implicated. Autophagy is activated during ventricular hypertrophy, serving to maintain cellular homeostasis. Excessive autophagy eliminates, however, essential cellular elements and possibly provokes cell death, which together contribute to hypertension-related heart disease.
Authors:
Zhao V Wang; Beverly A Rothermel; 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     Date:  2010-01-29
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  285     ISSN:  1083-351X     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-03-15     Completed Date:  2010-04-12     Revised Date:  2013-05-31    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  8509-14     Citation Subset:  IM    
Affiliation:
Department of Medicine (Cardiology), University of Texas Southwestern Medical Center, Dallas, Texas 75390-8573, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Autophagy / physiology*
Blood Pressure / physiology*
Cell Death
Heart Diseases / pathology*,  physiopathology*
Heart Failure / physiopathology
Humans
Hypertension / pathology*
Models, Biological
Phenotype
Reperfusion Injury
Risk Factors
Time Factors
Grant Support
ID/Acronym/Agency:
HL-072016/HL/NHLBI NIH HHS; HL-075173/HL/NHLBI NIH HHS; HL-080144/HL/NHLBI NIH HHS; HL-090842/HL/NHLBI NIH HHS; HL-097768/HL/NHLBI NIH HHS
Comments/Corrections

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