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Polystyrene microplastics drive chondrotoxicity in osteoarthritis through inducing ER stress and apoptosis via NFKB1 activation
Summary
Scientists found that tiny plastic particles called microplastics—already known to accumulate in human joints—can trigger a chain reaction that damages cartilage cells, worsening a protein called NFKB1 that drives inflammation and cell death. This research, done in cells rather than in people, suggests microplastic pollution could be a hidden contributor to osteoarthritis, the joint disease that causes pain and stiffness in millions of people, and it points to a possible drug target to block this damage in the future.
Polystyrene microplastics (PS-MPs), recognized as widespread environmental contaminants, have been identified within human articular tissues. However, their contribution to the pathogenesis of osteoarthritis (OA) remains incompletely understood. In this study, a combination of network toxicology and transcriptomic profiling was employed to pinpoint 30 core targets implicated in PS-MP-induced OA. Functional enrichment analyses indicated significant associations with inflammatory processes, endoplasmic reticulum (ER) stress, and apoptotic pathways. Through machine learning algorithms, six potential diagnostic biomarkers for early-stage OA were identified. Among these, NFKB1 emerged as a core target, with both molecular docking and dynamic simulations confirming its stable interaction with PS-MPs. Subsequent in vitro assays and single-cell RNA sequencing revealed that PS-MPs upregulate NFKB1 expression, thereby intensifying inflammation, ER stress, and chondrocyte apoptosis. Notably, pharmacological inhibition of NFKB1 using MD-1 mitigated these deleterious effects and preserved extracellular matrix integrity. These findings elucidate a mechanistic pathway by which PS-MPs contribute to OA progression through NFKB1-driven ER stress and apoptosis, providing novel perspectives on environmentally induced OA pathology and identifying a potential therapeutic target for countering PS-MP-related chondrotoxicity.