Free radical biology & medicineMay 20, 2026

Nanoplastic exposure may cause energy problems, inflammation, and aging in kidney tubule cells

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated May 21, 2026

Abstract

Oral administration of nanoplastic particles at 200 mg/kg/day to mice for six weeks led to tubular-specific kidney injury.

Chronic exposure to nanoplastic particles resulted in inflammatory and fibrotic responses in the kidneys.
Transcriptomic analysis showed a decrease in genes related to energy production in mitochondria, alongside an increase in inflammatory and fibrotic pathways.
Mitochondrial function was disrupted in renal tubular cells, indicated by impaired energy production and increased oxidative stress.
Mitochondrial damage was linked to activation of specific inflammatory signaling pathways, though inflammation and cellular aging appeared to be mechanistically distinct.
Prolonged exposure to nanoplastic particles was associated with pronounced cellular aging due to ongoing mitochondrial dysfunction.
Activation of a specific protein (PGC1α) improved mitochondrial function and reduced inflammation and cellular aging in both cell cultures and mice.

Simplified

Nanoplastic (NP) particles are emerging environmental contaminants with increasing concern regarding their potential impacts on human health; however, their effects on kidney function remain poorly understood. Here, we combined in vivo and in vitro approaches to investigate renal toxicity induced by chronic NP exposure. Oral administration of NPs (200 mg/kg/day) to mice for six weeks resulted in tubular-specific kidney injury accompanied by inflammatory and fibrotic responses. Transcriptomic profiling revealed coordinated downregulation of mitochondrial oxidative phosphorylation-related genes along with enrichment of inflammatory and fibrotic pathways in the kidney. Consistently, disrupted mitochondrial function in renal tubular epithelial cells, as evidenced by impaired oxidative phosphorylation, increased mitochondrial reactive oxygen species, and structural mitochondrial abnormalities. Mitochondrial damage was associated with activation of STING-dependent inflammatory signaling; pharmacological inhibition of STING attenuated inflammatory responses but did not suppress NP-induced cellular senescence, indicating mechanistic dissociation between inflammation and senescence. In contrast, prolonged NP exposure induced robust cellular senescence linked to sustained mitochondrial dysfunction. Activation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) restored mitochondrial function and suppressed both inflammatory signaling and cellular senescence in vitro. Importantly, pharmacological activation of PGC1α in NP-exposed mice mitigated mitochondrial damage, renal inflammation, senescence, and fibrotic remodeling in vivo. Collectively, these findings identify mitochondrial dysfunction as a central mechanism associated with NP-induced renal inflammation and senescence and provide mechanistic insight into the hazardous effects of NP exposure on the kidney.

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Competing interests

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

PubMed

Nanoplastic exposure may cause energy problems, inflammation, and aging in kidney tubule cells

Abstract

Full Text

Funding

Competing interests

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