Rectifying METTL4-Mediated N ⁶ -Methyladenine Excess in Mitochondrial DNA Alleviates Heart Failure

Abstract

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.