Commentary: MicroRNA-221/222 Family Counteracts Myocardial Fibrosis in Pressure Overload-Induced Heart Failure

Frontiers in Cardiovascular Medicine

Boris Schmitz¹ 

关键词: heart failure;    remodeling;    micoRNAs;    cardiac hypertrophy;    exercise;   

DOI  :  10.3389/fcvm.2018.00095

学科分类：心脏病和心血管学

来源: Frontiers

【 摘 要 】

Recently Verjans et al. (1) investigated the role of microRNA (miRNA)-221 and -222 in heart failure and cardiac remodeling. Using endomyocardial biopsies of patients with dilated cardiomyopathy (DCM) the authors found significantly reduced levels of miRNA-221-3p and -222-3p in patients with severe fibrosis compared to those with non-severe fibrosis. Subsequent investigations in mice suggested that inhibition of miRNA-221 and -222 aggravated pressure overload–induced heart failure potentially by targeting components of the transforming growth factor-beta (TGF-beta) pathway. The authors concluded that delivery of synthetic miRNA-221/-222 might be a future treatment option in heart failure (1). Since these results are partly in contradiction with earlier reports suggesting that elevated levels of miRNA-221 and -222 may actually cause heart failure, it might be worthwhile to look at the history of miRNA-221/-222 research in heart failure.

【 授权许可】

CC BY