Literature DB >> 22926488

Extracellular matrix and fibroblast communication following myocardial infarction.

Yonggang Ma1, Ganesh V Halade, Merry L Lindsey.   

Abstract

The extracellular matrix (ECM) provides structural support by serving as a scaffold for cells, and as such the ECM maintains normal tissue homeostasis and mediates the repair response following injury. In response to myocardial infarction (MI), ECM expression is generally upregulated in the left ventricle (LV), which regulates LV remodeling by modulating scar formation. The ECM directly affects scar formation by regulating growth factor release and cell adhesion and indirectly affects scar formation by regulating the inflammatory, angiogenic, and fibroblast responses. This review summarizes the current literature on ECM expression patterns and fibroblast mechanisms in the myocardium, focusing on the ECM response to MI. In addition, we discuss future research areas that are needed to better understand the molecular mechanisms of ECM action, both in general and as a means to optimize infarct healing.

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Year:  2012        PMID： 22926488      PMCID： PMC3518752          DOI： 10.1007/s12265-012-9398-z

Source DB:  PubMed          Journal:  J Cardiovasc Transl Res        ISSN： 1937-5387            Impact factor:   4.132


  91 in total

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4.  Matrix metalloproteinase-28 deletion amplifies inflammatory and extracellular matrix responses to cardiac aging.

Authors:  Yonggang Ma; Ying Ann Chiao; Jianhua Zhang; Anne M Manicone; Yu-Fang Jin; Merry L Lindsey
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Journal:  Physiol Rev       Date:  2007-10       Impact factor: 37.312

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8.  Increased expression of connective tissue growth factor in the infarct zone of experimentally induced myocardial infarction in rats.

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Review 5.  Cardiac Fibroblast Activation Post-Myocardial Infarction: Current Knowledge Gaps.

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