Document Detail


Membrane-associated matrix proteolysis and heart failure.
MedLine Citation:
PMID:  23287455     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The extracellular matrix (ECM) is a complex entity containing a large portfolio of structural proteins, signaling molecules, and proteases. Changes in the overall integrity and activational state of these ECM constituents can contribute to tissue structure and function, which is certainly true of the myocardium. Changes in the expression patterns and activational states of a family of ECM proteolytic enzymes, the matrix metalloproteinases (MMPs), have been identified in all forms of left ventricle remodeling and can be a contributory factor in the progression to heart failure. However, new clinical and basic research has identified some surprising and unpredicted changes in MMP profiles in left ventricle remodeling processes, such as with pressure or volume overload, as well as with myocardial infarction. From these studies, it has become recognized that proteolytic processing of signaling molecules by certain MMP types, particularly the transmembrane MMPs, actually may facilitate ECM accumulation and modulate fibroblast transdifferentiation; both are critical events in adverse left ventricle remodeling. Based on the ever-increasing substrates and diversity of biological actions of MMPs, it is likely that continued research about the relationship of left ventricle remodeling in this family of proteases will yield new insights into the ECM remodeling process and new therapeutic targets.
Authors:
Francis G Spinale; Joseph S Janicki; Michael R Zile
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review    
Journal Detail:
Title:  Circulation research     Volume:  112     ISSN:  1524-4571     ISO Abbreviation:  Circ. Res.     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2013-01-04     Completed Date:  2013-02-27     Revised Date:  2014-05-21    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  195-208     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Transdifferentiation
Extracellular Matrix / metabolism*
Fibrosis
Gene Expression Regulation, Enzymologic
Heart Failure / enzymology*,  genetics,  pathology,  physiopathology,  therapy
Hemodynamics
Humans
Matrix Metalloproteinases / genetics,  metabolism*
Myocardium / enzymology*,  pathology
Myofibroblasts / enzymology,  pathology
Prognosis
Signal Transduction
Substrate Specificity
Ventricular Remodeling*
Grant Support
ID/Acronym/Agency:
HL057952/HL/NHLBI NIH HHS; HL089944/HL/NHLBI NIH HHS; HL095608/HL/NHLBI NIH HHS; R01 HL057952/HL/NHLBI NIH HHS; R01 HL089944/HL/NHLBI NIH HHS; R01 HL095608/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
EC 3.4.24.-/Matrix Metalloproteinases
Comments/Corrections

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