After Sal B and Met treatment, the expression of TGF-β1, p-Smad3, and Smad3 in mouse myocardial tissue was significantly downregulated, whereas Smad7 was significantly upregulated (Fig. 2E, G), which indicated that Sal B significantly improved myocardial fibrosis in DCM mice by upregulating Smad7 to inhibit the TGF-β1 signaling pathway. Here, SMAD3 is linked to Myocardial fibrosis.