ArticleArchives of medical science : AMS2024
The role and underlying mechanism of dental pulp stem cell-derived exosomal miR-31 in the treatment of osteoarthritis by targeting mTOR to enhance chondrocyte autophagy levels.
Article in Archives of medical science : AMS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Adipose-cartilage communication via EV-Mito-mtDNA signaling promotes osteoarthritis progression.Science advances · 2026Article
- Research progress of cuproptosis, ferroptosis, apoptosis, and autophagy in knee osteoarthritis.Frontiers in cell and developmental biology · 2026Review
- HIF-1α-centered metabolic reprogramming in osteoarthritis: cell type-specific effects and intercellular crosstalk among chondrocytes, BMSCs, and macrophages.Frontiers in immunology · 2026Review
- The dual role of autophagy in cartilage degradation: from mechanisms to targeted therapeutics.Frontiers in cell and developmental biology · 2026Review
- M1 macrophage exosomes induce ferroptosis via MiR-582-5p-mediated ZBTB10 suppression in sepsis-induced acute kidney injury.Archives of medical science : AMS · 2026Article
- Exploring causal correlations between inflammatory response-related genes and osteoporosis: a Multi-Omics Mendelian Randomization Study.Archives of medical science : AMS · 2025Article
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Authors and funding
10 authors.
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Abstract
Introduction: Osteoarthritis is the most prevalent progressive musculoskeletal disease. It leads to functional impairment and decreased quality of life. However, the current treatments remain unsatisfactory. Recent studies have revealed that exosomes derived from mesenchymal stem cells offer a promising approach to improve the pathological changes in osteoarthritis, cartilage tissue, and chondrocyte homeostasis. Material and methods: In this Results: The study findings showed that a dental pulp stem cell could generate typical characteristic exosomes. The injection of DPSC-exosomes ameliorated destruction of cartilage, promoted matrix synthesis, inhibited cell apoptosis, and decreased the expression of catabolic factors. However, this effect was shown to be almost eliminated when miR-31 antagomir was injected. Conclusions: Furthermore, DPSC-exosomes show an ability to promote autophagy in chondrocytes through mTOR inhibition, in addition to reducing the mTOR luciferase activity. The ability of DPSC-exosomes to partially regulate autophagy was blocked upon inhibition of miR-31. In brief, DPSC-exosomes have a chondroprotective role in a mouse osteoarthritis model. The underlying mechanism is possibly related to miR-31-mediated suppression of the mTOR-autophagy pathway.
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