In the experimental myocardial infarction in the mouse model, absence of fibulin-2 prevents the development of progressive ventricular dysfunction and shows a significantly improved survival rate by attenuating upregulation of other ECM protein synthesis commonly required in wound healing process, MMP-2 activation, and TGF-β signaling, suggesting a regulatory role of fibulin-2 in ECM protein synthesis during scar formation after myocardial necrosis [132]. This evidence concerns the gene FBLN2 and myocardial infarction.