SMAD2 and myocardial infarction: As shown in Figure 5, in the myocardial border zone and renal interstitial tissue of patients with renal fibrosis after myocardial infarction, miR-1908-5p can inhibit the TGF-β1-smad2/3 signaling pathway by targeting TGF-β1 to reduce the key phosphorylation of intracellular signaling protein smad2/3, thereby alleviating organ fibrosis and improving organ function (1).