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CPT1 deficiency blocks autophagic flux to promote lipid accumulation induced by co-exposure to polystyrene microplastic and cadmium

Frontiers in Pharmacology 2025 3 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Zhixuan Chen, Huayi Qu, Jian Sun, Tao Wang, Yan Yuan, Jianhong Gu, Jianchun Bian, Zongping Liu, Hui Zou

Summary

Researchers found that combined exposure to polystyrene microplastics and cadmium in mice led to fat accumulation in the liver by blocking a cellular cleanup process called autophagy. The study identified a specific enzyme, CPT1, whose activation could alleviate both the fat buildup and the blocked autophagy pathway. The findings suggest that microplastics may worsen the toxic effects of heavy metals on liver health through shared metabolic pathways.

Polymers
Body Systems

In conclusion, the concurrent exposure of PS-MPs and Cd resulted in the blockage of hepatic lipid accumulation and autophagic pathway and further aggravated the toxic damage to the liver. Activation of CPT1 could alleviate the PS-MPs and Cd-induced lipid accumulation and autophagy pathway blockage thus reducing liver injury.

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