m6A-Mediated epitranscriptional reprogramming drives cardiac fibrosis by suppressing PGC-1α and boosting mitochondrial fission

Dysregulated mitochondrial fission drives pathological cell states in cardiac fibrosis, but its upstream regulatory mechanisms remain poorly understood. The role of epitranscriptomic regulation, particularly N6-methyladenosine (m6A) modification, in this process has not been defined. We employed integrated approaches including in vitro models of TGF-β1-stimulated cardiac fibroblasts, in vivo mouse models of isoproterenol-induced cardiac fibrosis, and analysis of human atrial fibrillation tissues