Genetic and pharmacological inhibition of METTL3 alleviates renal fibrosis by reducing EVL m6A modification through an IGF2BP2-dependent mechanism.

Wei-Jian NiHong ZhouHao LuNan-Nan MaBing-Bing HouWei LiFan-Xu KongJu-Tao YuRui HouJuan JinJia-Gen WenTao ZhangXiao-Ming Meng

Published in: Clinical and translational medicine (2023)

Collectively, the overactivated METTL3/EVL m6A axis is a potential target for renal fibrosis therapy, and the pharmacological inhibition of METTL3 activity by isoforsythiaside suggests that it is a promising anti-renal fibrosis agent.

Keyphrases

liver fibrosis
gene expression
genome wide
stem cells
mouse model
cell proliferation
bone marrow
climate change
binding protein
cell therapy