In line with this, using a mouse model of pressure overload-induced heart failure by TAC, we discovered that TGF-β pathway was significantly deregulated and the phosphorylation of Smad3 was almost completely blocked after STDP treatment, suggesting inhibiting the TGF-β/Smad signaling is mainly involved in the anti-cardiac fibrosis effects of STDP on CHF mice. This evidence concerns the gene SMAD3 and persistent truncus arteriosus.