METTL3 mediates Ang-II-induced cardiac hypertrophy through accelerating pri-miR-221/222 maturation in an m6A-dependent manner.

Rui ZhangYangyang QuZhenjun JiChunshu HaoYamin SuYuyu YaoWenjie ZuoXi ChenMingming YangGenshan Ma

Published in: Cellular & molecular biology letters (2022)

Our findings suggest that METTL3 positively modulates the pri-miR221/222 maturation process in an m6A-dependent manner and subsequently activates Wnt/β-catenin signaling by inhibiting DKK2, thus promoting Ang-II-induced cardiac hypertrophy. AAV9-mediated cardiac METTL3 knockdown could be a therapeutic for pathological myocardial hypertrophy.

Keyphrases

cell proliferation
high glucose
long non coding rna
diabetic rats
left ventricular
angiotensin ii
long noncoding rna
stem cells
endothelial cells