Extracellular matrix and fibroblast communication following myocardial infarction

J Cardiovasc Transl Res. 2012 Dec;5(6):848-57. doi: 10.1007/s12265-012-9398-z. Epub 2012 Aug 28.

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Animals
  • CCN Intercellular Signaling Proteins / metabolism
  • Cell-Matrix Junctions / metabolism*
  • Cell-Matrix Junctions / pathology
  • Cicatrix / metabolism
  • Cicatrix / pathology
  • Extracellular Matrix / metabolism*
  • Extracellular Matrix / pathology
  • Fibroblasts / metabolism*
  • Fibroblasts / pathology
  • Humans
  • Myocardial Infarction / metabolism*
  • Myocardial Infarction / pathology
  • Myocardium / metabolism*
  • Myocardium / pathology
  • Signal Transduction*

Substances

  • CCN Intercellular Signaling Proteins