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

作者：Wang, Ya; Ma, Wenhan; Lu, Shuai; Yan, LianHua; Hu, Fen; Wang, ZhaoHui^*; Cheng, Bo^*

来源：Biochemical and Biophysical Research Communications, 2018, 506(1): 130-136.

DOI：10.1016/j.bbrc.2018.09.092

• Experimental autoimmune myocarditis
• Cardiac fibrosis
• Androgen receptor
• microRNA-125b

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 (R)) could improve cardiac inflammation and fibrosis. Using Primary CFs, we demonstrated that ASC-J9 (R) 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.

• 出版日期2018-11-17
• 单位华中科技大学; 武汉大学