Myofibroblasts, matrix metalloproteinases, and extracellular matrix proteins play critical roles in regulating left ventricular remodeling and scar formation following myocardial infarction.
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.
Ma et al. (Wed,) conducted a review in Myocardial infarction and left ventricular remodeling. Extracellular matrix and myofibroblasts was evaluated. Myofibroblasts, matrix metalloproteinases, and extracellular matrix proteins play critical roles in regulating left ventricular remodeling and scar formation following myocardial infarction.
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