We found that the expression levels of TGF-β1, P-SMAD2, and P-SMAD3 were significantly decreased, whereas that of SMAD7 was significantly increased in 3PO mice compared with DMSO mice (Figure 4B,C), suggesting that the mechanism by which 3PO protects against myocardial fibrosis is related to inhibition of the TGF-β1/SMAD2/3 signaling pathway. This evidence concerns the gene SMAD2 and Myocardial fibrosis.