Document Detail

Implications of protease activation in cardiac dysfunction and development of genetic cardiomyopathy in hamsters.
MedLine Citation:
PMID:  22784245     Owner:  NLM     Status:  Publisher    
It has become evident that protein degradation by proteolytic enzymes, known as proteases, is partly responsible for cardiovascular dysfunction in various types of heart disease. Both extracellular and intracellular alterations in proteolytic activities are invariably seen in heart failure associated with hypertrophic cardiomyopathy, dilated cardiomyopathy, hypertensive cardiomyopathy, diabetic cardiomyopathy, and ischemic cardiomyopathy. Genetic cardiomyopathy displayed in different strains of hamsters provides a useful model for studying heart failure due to either cardiac hypertrophy or cardiac dilation. Alterations in the function of several myocardial organelles such as sarcolemma, sarcoplasmic reticulum, myofibrils, mitochondria, as well as extracellular matrix have been shown to be due to subcellular remodeling as a consequence of changes in gene expression and protein content in failing hearts from cardiomyopathic hamsters. In view of the increased activities of various proteases, including calpains and matrix metalloproteinases in the hearts of genetically determined hamsters, it is proposed that the activation of different proteases may also represent an important determinant of subcellular remodeling and cardiac dysfunction associated with genetic cardiomyopathy.
Alison L Müller; Darren Freed; Larry Hryshko; Naranjan S Dhalla
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-7-11
Journal Detail:
Title:  Canadian journal of physiology and pharmacology     Volume:  -     ISSN:  1205-7541     ISO Abbreviation:  -     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-7-12     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0372712     Medline TA:  Can J Physiol Pharmacol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
a Institute of Cardiovascular Sciences, St. Boniface Hospital Research Centre, 351 Tache Avenue, and Departments of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, MB R2H 2A6, Canada.
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