TGFB1 and Myocardial fibrosis: In summary, our data suggest that BEL can ameliorate myocardial fibrosis by inhibiting the proliferation and phenotypic transformation of CFs; and these inhibitory effects of BEL are related to the regulation of TGF-β/Smads and p38 pathway and prevention of NR4A1 cytoplasmic localization that negatively regulated TGF-β signaling in CFs.