Studies using a murine model of THBS1 genetic deletion suggested that, in cardiac remodeling after myocardial infarction, THBS1 limits the infarct expansion of the noninfarcted myocardium [44] and these benefits were delivered via activation of TGF-β, MMP inhibition, and CD47-mediated anti-inflammatory actions [45]. This evidence concerns the gene TGFB1 and myocardial infarction.