METTL3-mediated m6A modification of TNFAIP3 promotes endothelial to mesenchymal transition and atherosclerosis via the NF-κB/SNAIL signaling pathway.

ABSTRACT: Endothelial-mesenchymal transition (EndMT) is crucial in atherosclerosis (AS) development, but its molecular mechanisms remain incompletely understood. TNFAIP3 is a crucial negative regulator that plays a central role in inflammatory responses and immune responses by inhibiting the NF-κB signaling pathway. This study aims to investigate the molecular mechanisms by which TNFAIP3 regulates EndMT and the progression of AS, as well as to elucidate the role of METTL3-mediated m6A modification in this process. Through both in vivo and in vitro assays, we analyzed the expression of TNFAIP3 in endothelial cells during AS and EndMT. In vitro, we inhibited TNFAIP3 expression in endothelial cells to observe its impact on EndMT. In vivo, we investigated the effects of endothelial cell-specific TNFAIP3

SUBMITTER: Chen J 

PROVIDER: S-EPMC12702209 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature