[HTML][HTML] Myofibroblasts and the extracellular matrix network in post-myocardial infarction cardiac remodeling
Y Ma, LE de Castro Brás, H Toba, RP Iyer… - … -European Journal of …, 2014 - Springer
Pflügers Archiv-European Journal of Physiology, 2014•Springer
The cardiac extracellular matrix (ECM) fills the space between cells, supports tissue
organization, and transduces mechanical, chemical, and biological signals to regulate
homeostasis of the left ventricle (LV). Following myocardial infarction (MI), a multitude of
ECM proteins are synthesized to replace myocyte loss and form a reparative scar. Activated
fibroblasts (myofibroblasts) are the primary source of ECM proteins, thus playing a key role
in cardiac repair. A balanced turnover of ECM through regulation of synthesis by …
organization, and transduces mechanical, chemical, and biological signals to regulate
homeostasis of the left ventricle (LV). Following myocardial infarction (MI), a multitude of
ECM proteins are synthesized to replace myocyte loss and form a reparative scar. Activated
fibroblasts (myofibroblasts) are the primary source of ECM proteins, thus playing a key role
in cardiac repair. A balanced turnover of ECM through regulation of synthesis by …
Abstract
The cardiac extracellular matrix (ECM) fills the space between cells, supports tissue organization, and transduces mechanical, chemical, and biological signals to regulate homeostasis of the left ventricle (LV). Following myocardial infarction (MI), a multitude of ECM proteins are synthesized to replace myocyte loss and form a reparative scar. Activated fibroblasts (myofibroblasts) are the primary source of ECM proteins, thus playing a key role in cardiac repair. A balanced turnover of ECM through regulation of synthesis by myofibroblasts and degradation by matrix metalloproteinases (MMPs) is critical for proper scar formation. In this review, we summarize the current literature on the roles of myofibroblasts, MMPs, and ECM proteins in MI-induced LV remodeling. In addition, we discuss future research directions that are needed to further elucidate the molecular mechanisms of ECM actions to optimize cardiac repair.
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