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Microplastics induce osteoporosis via dose‐divergent mechanisms: Multi‐omics reveal metabolic compensation and inflammatory senescence
Original title: Microplastics induce osteoporosis via dose‐divergent mechanisms: Multi‐omics reveal metabolic compensation and inflammatory senescence
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Rats given high doses of polystyrene microplastics for four weeks showed bone loss, weaker bone-forming cells, and disrupted bone-resorbing cells, along with changes in metabolism and inflammation-linked aging processes. Lower doses caused minimal effects. Researchers identified two chemical changes that could serve as early markers of microplastic-related bone damage.
Osteoporosis is a major global skeletal disease. Accumulating evidence indicates that microplastics (MPs) may contribute to osteoporosis pathogenesis, although the underlying mechanisms remain unclear. Here, rats were exposed to low‐dose (0.13 mg/kg) or high‐dose (1.3 mg/kg) polystyrene MPs for 4 weeks. MP distribution in femoral heads was visualized using fluorescence microscopy, bone mineral density was measured, and integrated metabolomic‑proteomic profiling was performed, with differential proteins validated via RT‐qPCR. Low‑dose MPs exerted minimal effects on bone metabolism. In contrast, high‑dose MPs induced significant bone loss, suppressed osteoblast function, dysregulated osteoclast‑mediated resorption, and activated specific apoptotic and inflammation-induced senescence pathways not observed in the low‐dose group. Multi‑omics analysis revealed dose‑divergent disruption of lipid, amino acid, and energy metabolism, together with protein alterations associated with redox imbalance and bone remodeling. These results demonstrate a dose‑divergent transition from subclinical metabolic stress to overt osteotoxicity. Notably, the sustained upregulation of Pg 34:1 and quinic acid was identified as a potential metabolic signature of MP‑induced bone damage. Collectively, this study shows that MPs, as hazardous environmental pollutants, can induce osteoporosis via dose‑divergent mechanisms, and provides potential molecular targets and biomarkers for early risk assessment of MP‐associated skeletal disorders.
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