SMAD2 and Myocardial fibrosis: Specifically, upon binding with the TGF-β1 receptor on the surface of myocardial fibroblasts, TGF-β1 stimulates phosphorylation of downstream SMADs protein (mainly SMAD2/3) and translocation into the nucleus in combination with SMAD4, induces myocardial fibroblast proliferation, phenotypic transformation, and collagen synthesis and ultimately promotes extracellular matrix formation and myocardial fibrosis.