Rectifying METTL4-Mediated N 6 -Methyladenine Excess in Mitochondrial DNA Alleviates Heart Failure.
Fuyang ZhangLing ZhangGuangyu HuXiyao ChenHui LiuCongye LiXiong GuoChong HuangFangfang SunTongzheng LiZhe CuiYongzhen GuoWenjun YanYunlong XiaZhiyuan LiuZhen LinWeixun DuanLinhe LuXinyi WangZhengyang WangShan WangLing TaoPublished in: Circulation (2024)
Our findings identify a pivotal role of cardiomyocyte mtDNA 6mA and the corresponding methyltransferase, METTL4, in the pathogenesis of mitochondrial dysfunction and HF. Targeted suppression of METTL4 to rectify mtDNA 6mA excess emerges as a promising strategy for developing mitochondria-focused HF interventions.