Such a mechanism is likely multifactorial, as CMCs appear to secret a myriad of cardiotrophic factors (i.e., MMP2/3 and CCN family proteins) that may respectively function to both directly (i.e., proteolytic degradation of interstitial type I collagen) and indirectly (i.e., inhibition of myofibroblast collagen production) impede myocardial fibrosis (Figure 6)—actions that may improve ventricular compliance and, in turn, enhance myocardial contractility. Here, MMP2 is linked to Myocardial fibrosis.