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Updated: Jan 16, 2026
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Evaluating Therapeutic Interventions in the SHIP-deficient Mouse Model of Crohn Disease-like Ileitis and Fibrosis
Published on: October 14, 2025
405
YTHDF1 Drives Ferroptosis in Ulcerative Colitis via m6A-ACSL4 Stabilization.
Yanhong Lin1, Yanping Zhang2, Xiaojun Wang2
1School of Medical Nursing, Minxi Vocational & Technical College, Longyan, Fujian, China.
Summary
YTHDF1 protein promotes ulcerative colitis (UC) by increasing ferroptosis via ACSL4 mRNA stabilization. Targeting YTHDF1 may offer a new therapeutic strategy for UC treatment.
Area of Science:
- Gastroenterology
- Molecular Biology
- Immunology
Background:
- Ulcerative colitis (UC) is a chronic inflammatory bowel disease.
- The role of m6A reader protein YTHDF1 in UC pathogenesis is unclear.
- Ferroptosis, an iron-dependent cell death, may contribute to UC.
Purpose of the Study:
- Investigate YTHDF1's role in UC.
- Determine YTHDF1's involvement in ferroptosis via ACSL4 regulation.
- Explore YTHDF1 as a potential therapeutic target for UC.
Main Methods:
- Analysis of UC patient samples and colitis mouse models.
- Assessment of ferroptosis markers (ROS, lipid peroxidation, iron).
- RNA immunoprecipitation (RIP) and MeRIP assays to study YTHDF1-ACSL4 interaction.
Main Results:
- YTHDF1 was upregulated in UC patients and mice, correlating with disease severity.
- YTHDF1 knockdown reduced colitis severity and suppressed ferroptosis.
- YTHDF1 stabilizes ACSL4 mRNA through m6A modification, promoting ferroptosis.
Conclusions:
- YTHDF1 promotes UC pathogenesis by inducing ferroptosis through ACSL4 mRNA stabilization.
- YTHDF1 is a potential therapeutic target for ulcerative colitis.
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