Document Detail


Extracellular matrix turnover and signaling during cardiac remodeling following MI: causes and consequences.
MedLine Citation:
PMID:  19559709     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The concept that extracellular matrix (ECM) turnover occurs during cardiac remodeling is a well-accepted paradigm. To date, a multitude of studies document that remodeling is accompanied by increases in the synthesis and deposition of ECM components as well as increases in extracellular proteases, especially matrix metalloproteinases (MMPs), which break down ECM components. Further, soluble ECM fragments generated from enzymatic action serve to stimulate cell behavior and have been proposed as candidate plasma biomarkers of cardiac remodeling. This review briefly summarizes our current knowledge base on cardiac ECM turnover following myocardial infarction (MI), but more importantly extends discussion by defining avenues that remain to be explored to drive the ECM remodeling field forward. Specifically, this review will discuss cause and effect roles for the ECM changes observed following MI and the potential role of the ECM changes that may serve as trigger points to regulate remodeling. While the pattern of remodeling following MI is qualitatively similar but quantitatively different from various types of injury, the basic theme in remodeling is repeated. Therefore, while we use the MI model as the prototype injury model, the themes discussed here are also relevant to cardiac remodeling due to other types of injury.
Authors:
Rogelio Zamilpa; Merry L Lindsey
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2009-06-25
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  48     ISSN:  1095-8584     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-02-17     Completed Date:  2010-05-14     Revised Date:  2013-02-18    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  558-63     Citation Subset:  IM    
Copyright Information:
2009 Elsevier Ltd. All rights reserved.
Affiliation:
Cardiology Division, Department of Medicine, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, Mail Code 7872, San Antonio, TX 78229-3900, USA.
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MeSH Terms
Descriptor/Qualifier:
Extracellular Matrix / metabolism*
Matrix Metalloproteinases / metabolism
Models, Biological
Myocardial Infarction / metabolism,  physiopathology*
Signal Transduction / physiology
Ventricular Remodeling / physiology
Grant Support
ID/Acronym/Agency:
R01 HL075360/HL/NHLBI NIH HHS; R01 HL075360/HL/NHLBI NIH HHS; R01 HL075360-06/HL/NHLBI NIH HHS; R01 HL075360-09/HL/NHLBI NIH HHS; T32 HL07446/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
EC 3.4.24.-/Matrix Metalloproteinases
Comments/Corrections

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