ArticleJournal of nanobiotechnology2026
Metformin-pretreated synovial mesenchymal stem cell-derived exosomes alleviate osteoarthritis via the miR-1208/METTL3/NLRP3 axis.
Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundOsteoarthritis (OA) is a common degenerative joint disease that lacks effective reparative treatment methods. Exosomes derived from synovial mesenchymal stem cells (SMSC) have emerged as a promising acellular therapeutic approach due to their roles in immune modulation and tissue regeneration. Metformin, a commonly used anti-diabetic drug, has been shown to possess anti-inflammatory properties and enhance stem cell functionality. This study aims to explore the therapeutic potential and underlying mechanisms of metformin-pretreated SMSC-derived exosomes (M-EVs) in OA treatment.
methodsThis study first conducted a retrospective analysis of clinical data from OA patients to evaluate the impact of metformin on joint damage. Subsequently, in vitro experiments were performed to investigate the effects of M-EVs on chondrocyte proliferation, apoptosis, migration, and extracellular matrix (ECM) metabolism. In addition, the in vivo efficacy of M-EVs was assessed in a DMM mouse model. Differentially expressed miRNAs were identified using miRNA arrays, and the role of the miR-1208/METTL3/NLRP3 signaling pathway in the therapeutic effects of M-EVs was further elucidated using luciferase reporter assays, m⁶A measurements, and Western blot analyses.
resultsClinical data indicated that OA patients who had been on long-term metformin therapy exhibited less severe joint structural damage. In vitro experiments demonstrated that M-EVs, enriched in miR-1208, inhibited METTL3 expression and reduced m⁶A modification levels of NLRP3, thereby suppressing NLRP3 inflammasome activation and the release of pro-inflammatory factors. M-EVs significantly promoted chondrocyte proliferation and migration, reduced apoptosis, and improved ECM metabolism. Further animal studies confirmed that M-EVs effectively slowed OA progression, improved cartilage structure, and modulated the inflammatory microenvironment, with the therapeutic effect being dependent on the NLRP3 pathway.
conclusionMetformin-pretreated SMSCs enhance the anti-inflammatory and chondroprotective properties of their secreted exosomes, primarily through the miR-1208-mediated METTL3/NLRP3 signaling pathway. M-EVs offer an innovative, safe, and potentially translatable acellular therapeutic strategy for OA treatment.
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