It is worth noting that in the early stage of MI, increased expression of TGF-β1 promotes the recruitment of fibroblasts to the infarction site and secretion of collagen and other substances to promote the recovery of myocardial injury431; however, continued fibrotic responses cause cardiac remodeling and reduced heart function, which eventually lead to heart failure426. This evidence concerns the gene TGFB1 and myocardial infarction.