ArticleRenal failure2025
The m6A reader YTHDF2 protects vascular smooth muscle cells against the osteogenic differentiation through targeting Runx2.
Article in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Novel insights into the role of the renal interstitial microenvironment in Randall's plaque formation (Review).International journal of molecular medicine · 2026Review
- HSP90AA1 Facilitates Vascular Calcification in Chronic Kidney Disease Involving Chaperone-Mediated Autophagy.Biomedicines · 2026Article
- A Comprehensive Review of Epigenetic Regulation of Vascular Smooth Muscle Cells During Development and Disease.Biomolecules · 2026Review
- The Central Role of m6A as Epigenetic Regulator in Metabolic Disorders of Therapeutic Potential and Clinical Implications.Molecular neurobiology · 2025Review
- Knockdown of RGMa reduces vascular calcification by inhibiting the AKT signaling pathway.Scientific reports · 2025Article
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Authors and funding
9 authors.
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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
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