ArticleCellular and molecular life sciences : CMLS2025
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.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed.
- Research Advances on Mesenchymal Stem Cell-Derived Exosomes in Anti-Graft-Versus-Host Disease Therapy: Mechanisms, Therapeutic Potential, and Future Prospects.International journal of molecular sciences · 2026Review
- Review
- Expression Profiles, Biological Functions and Clinical Significance of Circular RNAs in Inflammatory Bowel Disease.Journal of inflammation research · 2026Review
- Exosomal non-coding RNAs in autoimmune diseases: molecular mechanisms and potential applications.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
objectiveUlcerative colitis (UC) is an inflammatory bowel disease that lacks satisfactory treatment. This study aimed to investigate the role of bone marrow mesenchymal stem cell-derived exosomal circHECTD1 (Exo-circHECTD1) in UC and its mechanism of action.
methodsAn inflammatory model was created using LPS-stimulated MODE-K cells and an UC mouse model was established using dextran sodium sulfate (DSS). Cell proliferation was assessed using CCK-8. Apoptosis and Th17/Treg cell differentiation were analyzed by flow cytometry. Inflammatory factors were detected using ELISA. FITC fluorescence intensity was measured to evaluate permeability. m
resultsExo-circHECTD1 enhanced viability and permeability and reduced apoptosis and inflammation factor levels in LPS-treated MODE-K cells. Moreover, it reduced the Th17/Treg ratio, regulated gut microbiota, and promoted the recovery of mice with DSS-induced UC. Claudin1 knockdown reversed the protective effect of Exo-circHECTD1 on UC models. CircHECTD1 binds to CTCF, which binds to the METTL3 promoter and promotes METTL3 promoter activity. METTL3 upregulates the level of claudin1 m
conclusionExo-circHECTD1 inhibits METTL3 transcription by binding to CTCF to reduce claudin1 m
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Registered trials
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