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Polystyrene microplastics drive chondrotoxicity in osteoarthritis through inducing ER stress and apoptosis via NFKB1 activation
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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.
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Microplastics as an emerging driver of osteoarthritis: a translational synthesis of environmental exposure, patho-mechanisms, and public health implications
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A translational synthesis of clinical and experimental data examined the role of microplastic exposure in osteoarthritis (OA) development, finding evidence that MPs bioaccumulate in joint tissues and may promote inflammation and oxidative damage that disrupts cartilage homeostasis. The review identified MP exposure as a plausible but underexplored contributor to OA progression.
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Researchers detected polystyrene microplastics in synovial fluid from rheumatoid arthritis patients and showed that 5 µm particles directly activated NF-κB and MAPK inflammatory signaling in joint fibroblasts, potentially amplifying synovial inflammation and joint destruction.
Integrating network toxicology and in vitro validation to elucidate PET microplastic-induced osteoarthritis pathogenesis
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Scientists found that PET microplastics — tiny plastic particles from common plastic bottles and packaging — may worsen osteoarthritis by triggering inflammation and damaging cartilage cells at the molecular level. Using computer modeling and lab tests on cartilage cells, they pinpointed six specific genes that get switched on or off when exposed to these plastic particles, offering early clues about how everyday plastic pollution might contribute to joint disease. While this is still early-stage lab research (not yet tested in humans), it adds to growing evidence that microplastics in our environment could have real effects on joint health.
Exploration of potential targets and toxicological mechanisms of microplastic exposure-induced osteoarthritis based on network toxicology, molecular docking and experimental validation
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Scientists found that tiny plastic particles (microplastics), which we regularly ingest through food and air, may damage joint cartilage and contribute to osteoarthritis by disrupting specific genes involved in inflammation and cell damage. Using computer modeling and lab experiments on cartilage cells, researchers also found that quercetin—a natural compound found in fruits and vegetables—may help protect against this damage, though more research is needed before it could be recommended as a treatment. This study adds to growing concerns about how everyday plastic exposure might affect joint health, while pointing toward a possible natural way to help defend against it.
Nanoplastics exposure accelerates the progression of osteoarthritis via lysosomal destabilization-mediated pyroptosis
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Researchers exposed osteoarthritis mouse models to 20-nm polystyrene nanoplastics in drinking water and found that particles accumulated in chondrocyte lysosomes, triggering lysosomal membrane permeabilization, cathepsin B release, and NLRP3-driven pyroptosis that accelerated cartilage degradation—with quercetin restoring lysosomal integrity and substantially reducing joint destruction.
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