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Microplastics induce osteoarthritis by modulating chondrocyte inflammation and disrupting TGF-β signaling in mesenchymal stem cells
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Researchers detected microplastics of varying types and sizes in the synovial fluid of osteoarthritis patients and showed in mice that chronic oral microplastic exposure triggers cartilage degeneration via IL-1β/SPP1 signaling in chondrocytes and disrupted TGF-β signaling in bone marrow stem cells, with pharmacological TGF-β inhibition significantly attenuating disease progression.
INTRODUCTION: Microplastics (MPs) are pervasive pollutants that can accumulate in the human body through the food chain. Osteoarthritis (OA) is the most common degenerative joint disease with an increasing prevalence due to global aging and obesity, both of which are closely influenced by dietary habits. However, the impact of MPs on OA pathogenesis remains unclear. OBJECTIVES: This study aimed to uncover the potential impact of MPs on OA development, elucidate the underlying mechanisms, and explore potential therapeutic strategies. METHODS: Different types and sizes of MPs in the synovial fluid from OA patients were analyzed. A chronic oral MPs exposure mouse model was established, with OA-like pathology evaluated by safranin-O/fast green (SOFG) staining and micro-CT. In vitro experiments using chondrocytes and bone marrow mesenchymal stem cells (BMSCs) assessed apoptosis, oxidative stress, chondrogenic differentiation, and molecular mechanisms. The role of TGF-β signaling as a systemic downstream target of MPs was further examined through in vivo pharmacological inhibition. RESULTS: MPs of various types and sizes were detected in the synovial fluid of patients with osteoarthritis of varying severity. Moreover, chronic oral MPs exposure in mice was associated with the development of OA-like features, including cartilage degeneration and subchondral bone destruction. Further experiments validated that MPs could induce apoptosis and oxidative stress in both chondrocytes and BMSCs while inhibiting chondrogenic differentiation. Mechanistic studies suggested that IL-1β/SPP1 signaling in chondrocytes and TGF-β signaling in BMSCs both contribute to the MPs-induced OA. In particular, pharmacological inhibition of TGF-β signaling significantly attenuates OA progression induced by MPs in mice. CONCLUSION: Our findings suggest that MPs may serve as a potential environmental risk factor associated with OA progression, offering experimental evidence that links microplastic pollution to the pathogenesis of OA. Furthermore, our results indicate that TGF-β signaling could be a potential target for intervening in MPs-induced OA.
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