ArticleCell death discovery2022
METTL3 overexpression aggravates LPS-induced cellular inflammation in mouse intestinal epithelial cells and DSS-induced IBD in mice.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
What it found
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Who cites it
67 citing papers in PubMed, 92 citations in OpenAlex.
- METTL3 Alleviates Liver Abscess by Enhancing Macrophage Efferocytosis via mImmunity, inflammation and disease · 2026Article
- METTL3 loss exacerbates colitis via mActa pharmacologica Sinica · 2026Article
- Epigenetic Alterations in Microbiome-Host Interactions in Inflammatory and Autoimmune Diseases.International journal of molecular sciences · 2026Review
- Matrine improves bile acid metabolism and reduces inflammatory and oxidative stress in colitis via the JAK2 pathway.Chinese medicine · 2026Article
- YTHDC2 Deficiency Exacerbates Ulcerative Colitis by Stabilizing RBMS1 mRNA to Drive Epithelial Ferroptosis.Inflammation · 2026Article
- METTL3-mCellular & molecular biology letters · 2026Article
- Deletion of Circadian Rhythms Gene BMAL1 Impairs the Intestinal Epithelial Barrier and Exacerbates Intestinal Inflammation by Inducing Pyroptosis.Mediators of inflammation · 2026Article
- A context-dependent METTL1-m7G-SLC7A11 axis links metabolic stress to epithelial fate in ulcerative colitis.International journal of biological sciences · 2026Article
- CD73 Blockade Aggravate Dextran-Sodium-Sulfate-Induced Colitis via Down Regulating Inosine.Journal of inflammation research · 2026Article
- Macrophage-Orchestrated Metabolic Sensing Drives IBD Pathogenesis: A Framework for Targeted Therapy.International journal of biological sciences · 2026Review
- Geniposide Alleviates Inflammatory Bowel Disease by Regulating Intestinal Flora and Arginine Metabolism and Inhibiting the NF-κB Pathway Through Targeting Anxa5.Mediators of inflammation · 2026Article
- Smad2/3 Regulates IL-6R m6A Methylation through METTL3 to Influence Inflammatory Responses in Hemorrhoidal Disease.Journal of innate immunity · 2026Article
- Epitranscriptomic regulation by m6A in immunity and autoimmune disorders: emerging mechanisms and clinical perspectives.Frontiers in immunology · 2026Review
- Gut microbiota-derived metabolites and IL-22 signaling in inflammatory bowel disease: context-dependent regulation of mucosal repair and inflammation.Frontiers in immunology · 2026Review
- The mFrontiers in cell and developmental biology · 2026Review
- Bone marrow mesenchymal stem cell-derived circHECTD1 targets claudin1 through the CTCF/METTL3 axis to alleviate ulcerative colitis : Short title: BMSC-derived circHECTD1 alleviates UC.Cellular and molecular life sciences : CMLS · 2025Article
- mCellular and molecular life sciences : CMLS · 2025Article
- Dysregulated programmed cell death of intestinal epithelial cells in ulcerative colitis: Molecular mechanisms and novel therapeutic interventions (Review).International journal of molecular medicine · 2025Review
- Review
- Astragaloside IV Alleviates Ulcerative Colitis Progression by Inhibiting WDR5-Mediated ENO1 H3K4me3 Modification.The Kaohsiung journal of medical sciences · 2025Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), are chronic inflammatory disorders of the intestine. Dysregulated cytokine secretion and signal transduction mechanisms via intestinal epithelial cells are involved in IBD pathogenesis, in which the transcription factor NF-κB plays a critical role. In this study, METTL3, which plays a key role in inflammation regulation, has been recognized significantly up-regulated in IBD samples, DSS-induced IBD mice, and LPS-treated MODE-K cells. Within LPS-treated MODE-K cells, METTL3 knockdown promoted cell viability, inhibited cell apoptosis, decreased apoptotic caspase3/9 cleavage, and decreased the levels of proinflammatory cytokines (IL-1β, TNF-α, IL-6, and IL-18) and inflammatory enzymes (COX-2 and iNOS). Under the same conditions, METTL3 knockdown inhibited, whereas METTL3 overexpression promoted p65 phosphorylation in MODE-K cells; NF-κB inhibitor JSH-23 partially abolished the promotive effects of METTL3 overexpression upon p65 phosphorylation. Consistently, the effects of METTL3 overexpression upon LPS-stimulated MODE-K cells were partially abolished by JSH-23. Lastly, METTL3 knockdown in DSS-induced IBD mice significantly ameliorated DSS-induced IBD and inhibited DSS-induced p65 phosphorylation. In conclusion, METTL3 overexpression aggravates LPS-induced cellular inflammation in mouse intestinal epithelial cells and DSS-induced IBD in mice. The NF-κB signaling might be involved, and the regulatory mechanism remains to be investigated in our future study.
Identifiers
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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.