Polylactic acid nanoplastics induce kidney injury by activating the TRPM2-mediated mitophagy pathway.

Authors

Ziwen Yan, Tiantian Jia, Yuankun Zhou, Hengyi Xu

Published in

Chemico-biological interactions. Pages 112385. Oct 12, 2026. Epub Oct 12, 2026.

Abstract

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.

PMID:
42863736
Bibliographic data and abstract were imported from PubMed on 13 Oct 2026.

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