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Polystyrene Microplastics Induce Nephrotoxicity via Oxidative Stress, Inflammation, Autophagy, and Ferroptosis
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Researchers reviewed the mechanisms by which polystyrene microplastics damage kidney tissue, finding that they converge on oxidative stress, NF-κB/NLRP3 inflammatory activation, and disruption of autophagy and ferroptosis pathways, with hub genes TP53 and TNF central to the toxic network and particle aging amplifying toxicity.
Polystyrene microplastics (PS-MPs), pervasive environmental pollutants, pose a significant concern for kidney health. This review synthesizes current evidence to elucidate their nephrotoxic mechanisms. PS-MPs induce renal injury primarily by triggering oxidative stress, activating inflammatory pathways (e.g., NF-κB/NLRP3), and disrupting programmed cell death processes including autophagy and ferroptosis. Protein-protein interaction analysis identifies key hub genes like TP53 and TNF within this toxic network. Importantly, toxicity is modulated by particle properties, environmental aging, and coexposures. We conclude by highlighting critical research gaps, particularly the need to define risks from long-term, low-dose exposure and to develop effective mitigation strategies.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.