TGFB1 and myocardial infarction: After MI, many macrophages accumulate at the site of myocardial injury, among which M2 macrophages activate cardiac fibroblasts into collagen-secreting myofibroblasts by releasing matrix metalloproteinase (MMP) [59] and TGF-β (serves as the master switch) regulating the transition from inflammation to fibrosis, which are involved in scar formation and cardiac fibrosis [7, 60, 61].