Alkbh5 promotes Ythdf1 expression through demethylation thereby facilitating Fth1 translation to inhibit ferroptosis of myocardial infarction.

ABSTRACT:

Background

Myocardial infarction (MI) is a leading cause of global mortality. Ferroptosis, an iron-dependent form of programmed cell death, has recently emerged as a critical player in cardiovascular diseases. N6-methyladenosine (m6A), the most prevalent RNA methylation modification in eukaryotic cells, has been implicated in various pathological processes; however, its regulatory role in MI through ferroptosis remains poorly understood. This study aimed to elucidate the mechanism by which m6A methylation mediates MI via ferroptosis.

Methods

A hypoxia/reoxygenation (H/R) model was established using H9C2 cells to simulate myocardial injury. RNA methylation levels were quantified via dot blot assay. Ferroptosis was evaluated by measuring lactate dehydrogenase (LDH) release, Fe

SUBMITTER: Yin M 

PROVIDER: S-EPMC12007164 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature