Document Detail


Exercise can prevent and reverse the severity of hypertrophic cardiomyopathy.
MedLine Citation:
PMID:  16439687     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hypertrophic cardiomyopathy (HCM) is the most common form of sudden death in young competitive athletes. However, exercise has also been shown to be beneficial in the setting of other cardiac diseases. We examined the ability of voluntary exercise to prevent or reverse the phenotypes of a murine model of HCM harboring a mutant myosin heavy chain (MyHC). No differences in voluntary cage wheel performance between nontransgenic (NTG) and HCM male mice were seen. Exercise prevented fibrosis, myocyte disarray, and induction of "hypertrophic" markers including NFAT activity when initiated before established HCM pathology. If initiated in older HCM animals with documented disease, exercise reversed myocyte disarray (but not fibrosis) and "hypertrophic" marker induction. In addition, exercise returned the increased levels of phosphorylated GSK-3beta to those of NTG and decreased levels of phosphorylated CREB in HCM mice to normal levels. Exercise in HCM mice also favorably impacted components of the apoptotic signaling pathway, including Bcl-2 (an inhibitor of apoptosis) and procaspase-9 (an effector of apoptosis) expression, and caspase-3 activity. Remarkably, there were no differences in mortality between exercised NTG and HCM mice. Thus, not only was exercise not harmful but also it was able to prevent and even reverse established cardiac disease phenotypes in this HCM model.
Authors:
John P Konhilas; Peter A Watson; Alexander Maass; Dana M Boucek; Todd Horn; Brian L Stauffer; Stephen W Luckey; Paul Rosenberg; Leslie A Leinwand
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2006-01-26
Journal Detail:
Title:  Circulation research     Volume:  98     ISSN:  1524-4571     ISO Abbreviation:  Circ. Res.     Publication Date:  2006 Mar 
Date Detail:
Created Date:  2006-03-03     Completed Date:  2006-03-30     Revised Date:  2013-02-07    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  540-8     Citation Subset:  IM    
Affiliation:
Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309-0347, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis
Cardiomyopathy, Hypertrophic / pathology,  prevention & control*,  therapy
Caspase 3
Caspases / metabolism
Cyclic AMP Response Element-Binding Protein / metabolism
Fibrosis
Glycogen Synthase Kinase 3 / metabolism
Male
Mice
Mice, Inbred C57BL
Myocardium / pathology
Myogenic Regulatory Factors / analysis
Myosin Heavy Chains / genetics
NFATC Transcription Factors / analysis
Phosphorylation
Physical Conditioning, Animal*
RNA, Messenger / analysis
Signal Transduction
Grant Support
ID/Acronym/Agency:
F32 HL 67543/HL/NHLBI NIH HHS; F32 HL 70509/HL/NHLBI NIH HHS; F32 HL 72565/HL/NHLBI NIH HHS; F32 HL067543/HL/NHLBI NIH HHS; F32 HL067543-01/HL/NHLBI NIH HHS; F32 HL070509/HL/NHLBI NIH HHS; HL 56510/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Creb1 protein, mouse; 0/Cyclic AMP Response Element-Binding Protein; 0/Mef2a protein, mouse; 0/Myogenic Regulatory Factors; 0/Myosin Heavy Chains; 0/NFATC Transcription Factors; 0/RNA, Messenger; EC 2.7.11.1/glycogen synthase kinase 3 beta; EC 2.7.11.26/Glycogen Synthase Kinase 3; EC 3.4.22.-/Casp3 protein, mouse; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases
Comments/Corrections
Comment In:
Circ Res. 2006 Mar 3;98(4):443-5   [PMID:  16514074 ]

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