ArticleStem cell research & therapy2025
Gingival mesenchymal stem cell-derived exosomal miR-23a-3p targets IL-6R to attenuate autoimmune insulitis: a cell-free therapeutic strategy for type 1 diabetes.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Applications and prospects of the immunomodulatory and regenerative capabilities of gingival mesenchymal stem cells for chronic inflammation treatment.Molecular biology reports · 2026Review
- Modified Shenqi compound alleviated constipation and inflammation in diabetic mice by regulating the miR-23a-3p/Nrf2 axis.Journal of molecular histology · 2026Article
- Exosomal non-coding RNAs in autoimmune diseases: molecular mechanisms and potential applications.Frontiers in immunology · 2026Review
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10 authors.
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Abstract
backgroundType 1 diabetes (T1D) is characterized by autoimmune destruction of pancreatic β-cells, yet current therapies fail to address immune dysregulation. Gingival mesenchymal stem cells (GMSC) exhibit immunomodulatory potential, but cell-based therapies face challenges in standardization and survival. Exosomes, nanosized vesicles delivering bioactive molecules like miRNAs, offer a cell-free alternative. This study investigates GMSC-derived EXO (GMSC-EXO) enriched with miR-23a-3p as a novel strategy to attenuate T1D progression.
methodsSpontaneous T1D in NOD/LtJ mice was treated with GMSC-EXO. Exosome secretion was inhibited using GW4869, and miR-23a-3p was knocked down via LV3-miR-23a-3p inhibitor. Blood glucose, pancreatic inflammation, and immune cell dynamics were monitored in vivo. CD4
resultsGMSC-EXO delayed hyperglycemia progression and improved survival. Depleting exosomes or miR-23a-3p diminished therapeutic efficacy. Mechanistically, miR-23a-3p directly silenced IL-6R, suppressing IL-6R/JAK1/STAT3 signaling, reducing Th1/Th17 infiltration, and expanding Tregs and IL-10 + cells. In vitro, GMSC-EXO reduced IFN-γ/IL-17 A and elevated IL-10, effects abolished by miR-23a-3p inhibition.
conclusionsGMSC-EXO deliver miR-23a-3p to target IL-6R, restoring immune balance and mitigating insulitis in T1D. This study highlights the miR-23a-3p/IL-6R axis as a therapeutic target and establishes GMSC-EXO as a safe, cell-free strategy for autoimmune disorders. These findings provide a foundation for engineering exosome-based therapies in diabetes and related conditions.
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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 Socratic graph.