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Polylactic acid nanoplastics induce kidney injury by activating the TRPM2-mediated mitophagy pathway.
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Mice given polylactic acid nanoparticles by mouth for 28 days developed kidney damage, with higher doses causing worse injury. The damage involved a cell receptor called TRPM2 and a process called mitophagy, and mice lacking TRPM2 or given a mitophagy-blocking drug showed less kidney injury.
Polylactic acid nanoparticles (PLA NPs) are widely used biodegradable plastics, but their potential health risks remain unclear. This study explores whether PLA NPs induce renal cell apoptosis through a mitochondrial pathway involving transient receptor potential melastatin 2 (TRPM2) and mitophagy. Adult male C57BL/6 mice were orally exposed to 0.1, 1, and 10 mg/kg/day PLA NPs for 28 consecutive days. PLA NPs caused dose-dependent kidney injury, with the high-dose group (group H, 10 mg/kg/day) showing the most severe renal apoptosis and functional impairment. In group H, renal calcium ion (Ca2+) levels, mitophagy, and TRPM2 expression were significantly elevated. To investigate the mechanism, TRPM2-KO mice (group KH) and mitophagy inhibitor Mdivi-1-treated mice (group Md) were orally administered 10 mg/kg/day PLA NPs daily. Compared with group H, both group KH and group Md showed reduced renal injury, as evidenced by decreased apoptosis and restored mitochondrial function. These results indicate that PLA NPs induce oxidative stress, activate the TRPM2 channel, cause calcium overload and excessive mitophagy, and ultimately trigger renal cell apoptosis. This study provides a theoretical basis for targeted treatment of kidney diseases caused by PLA NPs.
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Nephrotoxicity induced by PLA NPs and CuSO4: Crosstalk between Cu metabolism and ferroptosis via ATP7B autophagy.
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Researchers exposed mice to polylactic acid nanoplastics and copper sulfate together and found that the nanoplastics triggered autophagy-mediated degradation of the copper transporter ATP7B in kidney cells, causing copper overload that activated ferroptosis and structural glomerular damage—a previously unknown link between biodegradable nanoplastics and metal-induced kidney injury.
Synergistic kidney toxicity of polylactic acid nanoplastics and Cr(VI): Ferroptosis aggravated by mitophagy
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Researchers investigated the combined kidney toxicity of polylactic acid nanoplastics and hexavalent chromium in mice. The study found that co-exposure produced synergistic kidney damage through ferroptosis aggravated by mitophagy, suggesting that even bioplastic-derived nanoplastics can enhance heavy metal toxicity when both contaminants are present together.
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.
Toxicological effects and mechanisms of renal injury induced by inhalation exposure to airborne nanoplastics
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Researchers studied what happens to mouse kidneys after breathing in airborne polystyrene nanoplastics and found the particles accumulated in kidney tissue after entering through the lungs. The nanoplastics activated stress and inflammation pathways that led to kidney cell damage and death. Testing on lab-grown human kidney organoids showed they were even more sensitive to nanoplastic exposure than standard cell lines, suggesting developing kidneys in embryos could be particularly vulnerable.
Micro- and nanoplastics and the kidney: exposure pathways, toxicokinetics, and pathophysiological insights
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Tiny plastic particles from our air, water, and food—called micro- and nanoplastics—can enter our bodies and travel to the kidneys, where studies show they may cause cell damage, inflammation, and scarring over time. This review pulls together existing research on how these plastics get into our system and harm kidney tissue, suggesting that everyday plastic exposure could be an overlooked risk factor for kidney disease. More research is needed, but this is an early signal that reducing plastic exposure might matter for long-term kidney health.
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