METTL3 Silencing Suppresses Cardiac Fibrosis Post Myocardial Infarction via m6A Modification of SMOC2.

ABSTRACT: Cardiac fibrosis, especially in the infarct border zone, leads to decreased cardiac compliance, impaired systolic and diastolic function, resulting in heart failure. M6A methylation plays a role in fibrosis development. However, its underlying mechanism remains poorly understood. This study explores the role and molecular mechanisms of m6A methylation in regulating cardiac fibrosis after myocardial infarction (MI). A mouse myocardial fibrosis model post-MI was established by ligating the left coronary artery. Corresponding gene knockdown was achieved in vitro or in vivo using short hairpin RNA or fibroblast-specific AAV9 virus. Echocardiography assessed cardiac function in mice, while Masson staining determined the degree of collagen deposition post-MI. The meRIP-Seq kit detected mRNA meth

SUBMITTER: He Y 

PROVIDER: S-EPMC12413310 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature