ArticleJournal of orthopaedic translation2026
Semaglutide alleviates osteoarthritis independent of weight loss via GLP-1R-mediated activation of autophagy through AKT/mTOR inhibition.
Article in Journal of orthopaedic translation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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1 citing paper in PubMed.
- Emerging mechanisms and translational advances in musculoskeletal diseases.Journal of orthopaedic translation · 2026Article
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11 authors.
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Abstract
Objective: The development of osteoarthritis (OA) is closely associated with systemic metabolic disorders, yet there remains a lack of disease-modifying therapeutic strategies that simultaneously target metabolic abnormalities and inflammatory responses. This study aims to systematically evaluate the therapeutic potential of semaglutide, a long-acting glucagon-like peptide-1 receptor (GLP-1R) agonist used for diabetes management, in OA and to elucidate its underlying molecular mechanisms. Methods: We utilized a zebrafish cartilage injury repair model to screen and assess the impact of several hypoglycemic drugs on cartilage regeneration. OA was induced in C57BL/6 mice by destabilization of the medial meniscus (DMM) surgery. Using systemic Results: Drug screening using a zebrafish cartilage injury model demonstrated that semaglutide exerted the most significant pro-regenerative effects, markedly promoting cartilage repair. In wild-type (WT) mice with DMM-induced OA, semaglutide treatment significantly improved gait abnormalities and mechanical hyperalgesia without significantly affecting body weight, and alleviated cartilage destruction, synovitis, and subchondral bone sclerosis associated with abnormal chondrocyte metabolism. However, GLP-1R inhibition or Conclusion: Semaglutide exerts protective effects against OA by activating GLP-1R in chondrocytes, inhibiting the AKT/mTOR pathway, and enhancing chondrocyte autophagy. It alleviates abnormal cartilage metabolism in OA independently of body weight changes.
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