YTHDC2 promotes sepsis-induced cardiomyopathy by activating apoptosis and NF-κB pathway.

ABSTRACT: Sepsis-induced cardiomyopathy (SICM) is a severe complication of sepsis, especially in children, and identification of novel therapeutic targets remains essential for improving patient outcomes. Recent studies have implicated N6-methyladenosine (m⁶A), an RNA epigenetic modification, in SICM pathogenesis. However, the role of YTH domain-containing 2 (YTHDC2), an m⁶A reader protein, in SICM remains unclear. This study used lipopolysaccharide (LPS)-treated adolescent rats, primary cardiomyocytes and H9c2 cardiomyocytes to mimic SICM in vivo and in vitro. We observed a significant upregulation of YTHDC2 in vivo and in vitro. Through comprehensive analyses including RNA sequencing (RNA-seq), Western blotting, and flow

SUBMITTER: Wang W 

PROVIDER: S-EPMC12688274 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature