ArticleAtherosclerosis plus2026
YTHDF1 aggravates the progression of atherosclerosis by enhancing BRD4 mRNA stability and promoting EndMT transition in an m6A-Dependent manner.
Article in Atherosclerosis plus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background and objective: Endothelial-to-mesenchymal transition (EndMT) is a crucial process driving vascular remodeling in atherosclerosis (AS). N6-methyladenosine (m6A) RNA methylation, regulated by YTH N6-methyladenosine RNA binding protein F1 (YTHDF1), an m6A reader that modulates RNA stability and translation, influences various cellular functions, but its specific role in AS-related EndMT remains unclear. This study aimed to investigate the role of the m6A reader YTHDF1 in AS progression, focusing on its regulation of bromodomain containing 4 (BRD4), a central epigenetic regulator in the Bromodomain and Extra-Terminal (BET) family, and subsequent promotion of EndMT. Methods: Human AS datasets (involving 6 clinical samples in GSE97210 and 104 clinical samples in GSE100927) and single-cell RNA sequencing data from Apoe-/- mice (n = 3 in total) were analyzed to assess YTHDF1 expression and correlation. YTHDF1-/-Apoe-/- mice (n = 5) were generated and fed a high-fat diet to evaluate plaque formation. In vitro, human umbilical vein endothelial cells (HUVECs) were used for gain/loss-of-function experiments. Methylated RNA immunoprecipitation (MeRIP), RNA immunoprecipitation (RIP), site-directed mutagenesis, and functional assays (Transwell, wound healing) were employed to elucidate the molecular mechanism. Results: YTHDF1 was significantly upregulated in human AS plaques (P < 0.001) and positively correlated with EndMT markers. ScRNA-seq analysis revealed a progressive increase in YTHDF1-expressing endothelial cells during plaque progression in Apoe Conclusion: Our findings uncover a novel pathogenic axis in AS where YTHDF1, by recognizing METTL3-mediated m6A modification on BRD4 mRNA, enhances its stability. This leads to increased BRD4 expression, which in turn drives EndMT and exacerbates disease progression. The YTHDF1-m6A-BRD4 pathway may represent a potential therapeutic target for AS which requires further preclinical validation.
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