Main content area

Androgen receptor regulates cardiac fibrosis in mice with experimental autoimmune myocarditis by increasing microRNA-125b expression

Wang, Ya, Ma, Wenhan, Lu, Shuai, Yan, LianHua, Hu, Fen, Wang, ZhaoHui, Cheng, Bo
Biochemical and biophysical research communications 2018 v.506 no.1 pp. 130-136
androgen receptors, cardiomyopathy, collagen, fibrosis, inflammation, mice, myocarditis, patients, therapeutics
Cardiac fibrosis is an important cardiac remodeling event in the development of inflammation dilated cardiomyopathy (iDCM). We have previously observed that degradation enhancer of androgen receptor (ASC-J9®) could improve cardiac inflammation and fibrosis. Using Primary CFs, we demonstrated that ASC-J9® attenuates the expression of miR-125b, which subsequently inhibits the generation of collagen. In contrast, overexpressed AR in CFs induced collagen production, increases mir-125b.We also found that inhibition of miR-125b attenuates fibrosis which induced by the overexpression of AR. Our results indentify the functional role for AR as a regulator of cardiac fibrosis due to myocarditis and further show that AR exerts its effect by increasing microRNA-125b expression. Treatment with degradation enhancer of AR limits cardiac fibrosis in iDCM, thereby providing potentially a therapeutic approach for patients with iDCM.