SMAD2 and Myocardial fibrosis: The suppressive effect of α1-AR blockage on NE-induced differentiation of cardiac fibroblasts is associated with restraining PKC-p38-Smad2/3 signaling pathway, and restoring CHIP expression that downregulates TGF-BR1 and further suppresses Smad2/3 activation, resulting in alleviating LPS-caused myocardial fibrosis (Fig. 8).