Compared with the control (Yang et al., 2019) SCE administration in vivo significantly increased the survival rate of mice after MI; inhibited myocardial inflammation; reduced the levels of H3K4 trimethylation (H3K4me3) and H3K36 trimethylation (H3K36me3) in the Smad3 promoter; and inhibited the expression of CoL-I, CoL-IIII and Sma RNA and protein, indicating that the reduction in MF caused by SCE was related to the downregulation of TGF-β1/Smad3 signal transduction. Here, SMAD3 is linked to myocardial infarction.