ArticleEuropean journal of medical research2025
METTL14 modulates the progression and ferroptosis of colitis by regulating the stability of m6A-modified GPX4.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Mechanistic Networks, Cellular Specificity, and Therapeutic Opportunities of Ferroptosis in Ulcerative Colitis.Pharmaceuticals (Basel, Switzerland) · 2026Review
- METTL3/YTHDF1 drives M1 macrophage polarization and aggravates ulcerative colitis progression by regulating m6A modification of SerpinB5 mRNA and FBXO32-dependent NF-κB pathway.Journal of gastroenterology · 2026Article
- Ononin combined withBiochemistry and biophysics reports · 2026Article
- Akkermansia muciniphila affects colitis by inhibiting ferroptosis signaling pathway.Scientific reports · 2026Article
- Epitranscriptomic regulation by m6A in immunity and autoimmune disorders: emerging mechanisms and clinical perspectives.Frontiers in immunology · 2026Review
- mCellular and molecular life sciences : CMLS · 2025Article
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Authors and funding
5 authors.
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Abstract
Ulcerative colitis (UC) is non-specific inflammatory bowel disease. UC development and progression were closely associated with epigenetic modifications. Nevertheless, the specific relationship between N6-methyladenosine (m6A) modification at RNA transcription levels and UC pathogenesis remains unclear. We established UC cell models and mouse models through dextran sulfate sodium (DSS) induction. The expression levels of METTL14 were analyzed via qRT-PCR and western blot. In vitro functional experiments evaluated the effects of METTL14 overexpression on the viability of DSS-induced NCM460 cells and ferroptosis markers. Use of the m6A methylation detection kit, MeRIP-qPCR, and RNA stability experiments confirmed the molecular mechanism controlled by METTL14. In vivo experiments with inflammatory mice models elucidated the interaction between METTL14 and GPX4. Findings from this study indicated a notable reduction in m6A methyltransferase METTL14 expression in DSS-induced NCM460 cells and DSS-induced mice models. METTL14 overexpression effectively suppressed ferroptosis in DSS-induced NCM460 cells. In addition, METTL14 enhanced GPX4 mRNA stability through mediating m6A modification, and the interplay between METTL14 and GPX4 through m6A modification introduced innovative therapeutic approaches for UC management.
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