New insights into the central sympathetic hyperactivity post-myocardial infarction: Roles of METTL3-mediated m⁶ A methylation.

ABSTRACT: Ventricular arrhythmias (VAs) triggers by sympathetic nerve hyperactivity contribute to sudden cardiac death in myocardial infarction (MI) patients. Microglia-mediated inflammation in the paraventricular nucleus (PVN) is involved in sympathetic hyperactivity after MI. N6-methyladenosine (m⁶ A), the most prevalent mRNA and epigenetic modification, is critical for mediating cell inflammation. We aimed to explore whether METTL3-mediated m⁶ A modification is involved in microglia-mediated sympathetic hyperactivity after MI in the PVN. MI model was established by left coronary artery ligation. METTL3-mediated m⁶ A modification was markedly increased in the PVN at 3 days after MI, and METTL3 was primarily located in microglia by immunofluorescence. RNA-seq, MeRIP

SUBMITTER: Qi L 

PROVIDER: S-EPMC8831944 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature