SMAD2 and Myocardial fibrosis: The data in this study supported that prazosin inhibited the phosphorylation of PKC, p38, and Smad2/3 in the myocardium of mice injected with LPS and in NE-stimulated cardiac fibroblasts, demonstrating that the inhibitory effect of prazosin on NE-mediated cardiac fibroblasts differentiation was related to the blocking of PKC-p38-Smad2/3 signaling pathway, thereby alleviating LPS-induced myocardial fibrosis.