FTO suppresses cardiac fibrosis after myocardial infarction via m⁶A-mediated epigenetic modification of EPRS.

ABSTRACT:

Background

Cardiac fibrosis is common in myocardial infarction (MI), leading to progressive cardiac dysfunction. Studies suggested that the abnormal N⁶-methyladenosine (m⁶A) modification induced by fat mass and obesity protein (FTO) is vital in MI. However, the effects of FTO on post-infarction cardiac fibrosis have not been detected.

Methods

Western blot and quantitative real-time PCR were performed to detect the expression of FTO in the fibrotic tissue of rats. The functions of FTO on collagen biosynthesis were analyzed in vitro and in vivo. The underlying targets of FTO were selected through RNA-seq with m⁶A-seq. The following dual luciferase reporter assay and RNA stability assay were conducted to investigate the mechanisms of FTO-mediate

SUBMITTER: Wang J 

PROVIDER: S-EPMC11562098 | biostudies-literature | 2024 Nov

REPOSITORIES: biostudies-literature