Pharmacological studies have shown that baicalin can effectively inhibit myocardial fibrosis caused by various reasons by regulating peroxisome proliferators activated recepotor α/β/δ expression, p38 MAPK phosphorylation, AMPK/TGF-β/Smads signaling pathway, TGF β1/Smad2 signaling pathway, and other mechanisms [35–38]. Here, SMAD2 is linked to Myocardial fibrosis.