ArticleCellular & molecular immunology2024
Inhibition of METTL3 in macrophages provides protection against intestinal inflammation.
Article in Cellular & molecular immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 22 citations in OpenAlex.
- Gut-derived genistein fromGut microbes · 2026Article
- The gut microbiota-tryptophan metabolism-immune axis in inflammatory bowel disease: Mechanisms and therapeutic prospects.Human vaccines & immunotherapeutics · 2026Review
- RNA mActa pharmacologica Sinica · 2026Review
- METTL7A-Dependent mMedComm · 2026Article
- AL398, A Novel NSUN6 Inhibitor, Attenuates Epithelial-Mesenchymal Transition and Metastasis in Endometrial Cancer by Abrogating m5C-Dependent Stabilization of Snail mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Senkyunolide I Inhibits mtDNA-cGAS-STING Signaling in Macrophages via Targeting VDAC1 Oligomerization to Attenuate Ulcerative Colitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PRAS40-driven pro-inflammatory macrophage polarization is required for inflammatory bowel disease.Cell death & disease · 2026Article
- The Role of NMedComm · 2026Review
- Pre-clinical anti-tumor activity and preliminary safety of METTL3 inhibitors STM2457 and UZH1a in neuroblastoma.Translational cancer research · 2026Article
- Smad2/3 Regulates IL-6R m6A Methylation through METTL3 to Influence Inflammatory Responses in Hemorrhoidal Disease.Journal of innate immunity · 2026Article
- Macrophage-Orchestrated Metabolic Sensing Drives IBD Pathogenesis: A Framework for Targeted Therapy.International journal of biological sciences · 2026Review
- Methyltransferase-Like 3 Inhibition-Activated cGAS/STING Axis Enhances Immunotherapy and Poly(ADP-Ribose) Polymerase Inhibitor Sensitivity in Lung Adenocarcinoma.Research (Washington, D.C.) · 2026Article
- Review
- Research Progress on the Relationship Between the Intestinal Barrier and Macrophages.Current issues in molecular biology · 2025Review
- Review
- METTL3-mediated mActa biochimica et biophysica Sinica · 2025Article
- METTL3-mediated m6A modification in sepsis: current evidence and future perspectives.Epigenomics · 2025Review
- Macrophages: emerging targets for ulcerative colitis.Frontiers in immunology · 2025Review
- Roles of METTL3 and NLRP3 in pyroptosis and prospects in SCIRI.Frontiers in immunology · 2025Review
- RNA modification: a promising code to unravel the puzzle of autoimmune diseases and CD4Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammatory bowel disease (IBD) is prevalent, and no satisfactory therapeutic options are available because the mechanisms underlying its development are poorly understood. In this study, we discovered that increased expression of methyltransferase-like 3 (METTL3) in macrophages was correlated with the development of colitis and that depletion of METTL3 in macrophages protected mice against dextran sodium sulfate (DSS)-induced colitis. Mechanistic characterization indicated that METTL3 depletion increased the YTHDF3-mediated expression of phosphoglycolate phosphatase (PGP), which resulted in glucose metabolism reprogramming and the suppression of CD4+ T helper 1 (Th1) cell differentiation. Further analysis revealed that glucose metabolism contributed to the ability of METTL3 depletion to ameliorate colitis symptoms. In addition, we developed two potent small molecule METTL3 inhibitors, namely, F039-0002 and 7460-0250, that strongly ameliorated DSS-induced colitis. Overall, our study suggests that METTL3 plays crucial roles in the progression of colitis and highlights the potential of targeting METTL3 to attenuate intestinal inflammation for the treatment of colitis.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.