ArticleCell biology and toxicology2024
hucMSC-Ex alleviates inflammatory bowel disease in mice by enhancing M2-type macrophage polarization via the METTL3-Slc37a2-YTHDF1 axis.
Article in Cell biology and toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- RNA mActa pharmacologica Sinica · 2026Review
- Engineering immune cell therapies for inflammatory bowel disease: from stem cells to CAR T cells.Nature reviews. Gastroenterology & hepatology · 2026Review
- Tissue-Resident Macrophage in Inflammation and Cancer.MedComm · 2026Review
- Mechanistic Networks, Cellular Specificity, and Therapeutic Opportunities of Ferroptosis in Ulcerative Colitis.Pharmaceuticals (Basel, Switzerland) · 2026Review
- HucMSC-derived exosomes alleviate inflammatory bowel disease via upregulating FXR to suppress macrophage ferroptosis.Biology direct · 2026Article
- Exosomes derived from human umbilical cord mesenchymal stem cells attenuate neuroinflammation in intracerebral hemorrhage rats by modulating lactylation modification.Journal of translational medicine · 2026Article
- YTHDC2 Deficiency Exacerbates Ulcerative Colitis by Stabilizing RBMS1 mRNA to Drive Epithelial Ferroptosis.Inflammation · 2026Article
- RNA modifications in intestinal macrophages: Implications for gut immunity and inflammation.Genes & diseases · 2026Review
- Mesenchymal Stem Cells Derived Extracellular Vesicles in Inflammatory Bowel Disease: Therapeutic Efficacy and Bioengineering Applications.International journal of nanomedicine · 2026Review
- mFrontiers in immunology · 2026Review
- Application of Human Umbilical Cord Mesenchymal Stem Cells and Their Derived Exosomes in Gastrointestinal Diseases.International journal of nanomedicine · 2026Review
- Smad2/3 Regulates IL-6R m6A Methylation through METTL3 to Influence Inflammatory Responses in Hemorrhoidal Disease.Journal of innate immunity · 2026Article
- Roles of RNA-binding proteins in macrophage function regulation and immunotherapy.Frontiers in cell and developmental biology · 2026Review
- Activation of the RSAD2-YTHDF1 axis in smooth muscle causes inflammatory bowel disease via intercellular mitochondrial transfer.Nature communications · 2025Article
- Piceatannol Attenuates Benzo[Journal of agricultural and food chemistry · 2025Article
- Advances of exosome regulating‑FXR to repair inflammatory bowel disease (Review).International journal of molecular medicine · 2025Review
- Therapeutic Effect of Membrane Vesicle Drug Delivery Systems in Inflammatory Bowel Disease.Pharmaceutics · 2025Review
- Mesenchymal stem/stromal cells-derived exosomes: possible therapeutic mechanism in inflammatory bowel disease.Human cell · 2025Review
- The Role of microRNAs in Inflammatory Bowel Disease.International journal of molecular sciences · 2025Review
- Efficacy of umbilical cord-derived mesenchymal stem cells and exosomes in conjunction with standard IBD drug on immune responses in an IBD mouse model.Stem cell research & therapy · 2025Article
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Authors and funding
6 authors.
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Abstract
Human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Ex) have emerged as a new treatment strategy for inflammatory bowel disease (IBD) due to their immunoregulatory function. N6-methyladenosine (m6A) plays a crucial role in regulating intestinal immunity, especially in IBD where macrophages play an important role, although its mechanism is not yet fully understood. From this perspective, this research aimed to evaluate the effect of hucMSC-Ex on m6A modification of macrophages in IBD. In the process of alleviating inflammation, hucMSC-Ex promotes macrophage polarization toward the M2 type and regulates intracellular m6A levels by upregulating the expression of m6A "Writer" METTL3 and "Reader" YTHDF1. Solute Carrier Family 37 Member 2 (Slc37a2) was identified by Methylation RNA immunoprecipitation sequencing as the target molecule of the hucMSC-Ex. Mechanically, hucMSC-Ex promoted the binding of METTL3 to the Slc37a2 mRNA complex, and enhanced the binding of Slc37a2 to YTHDF1 to upregulate the intracellular expression of Slc37a2, thereby attenuating the pro-inflammatory function of macrophage. This study confirms the modulatory role of hucMSC-Ex on the m6A modification of macrophages in IBD, providing a new scientific basis for the treatment of IBD with hucMSC-Ex.
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