The m6A reader YTHDF2 protects vascular smooth muscle cells against the osteogenic differentiation through targeting Runx2.

ABSTRACT: Vascular calcification (VC) is an important pathological development progress in chronic kidney disease (CKD) and may increase mortality but lacks effective treatments. N6-methyladenosine (m6A) has been verified to be the most prevalent internal chemical RNA modification in mammalian mRNAs. The M6A-modified mRNA degradation process is mediated by the reader YTHDF2 in an m6A-dependent manner. Nevertheless, the exact role and molecular mechanism of YTHDF2 in VC remain unclear. This study aimed to investigate the potential role of YTHDF2 in the osteogenic differentiation of vascular smooth muscle cells (VSMCs). It was found that YTHDF2 was markedly downregulated in both in vivo and in vitro calcified models. Functionally, YTHDF2 plays a protective role in VC. The overexpression

SUBMITTER: Li L 

PROVIDER: S-EPMC12001846 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature