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环境纳米塑料诱导线粒体功能障碍:细胞机制及相关疾病综述

Environmental nanoplastics induce mitochondrial dysfunction: A review of cellular mechanisms and associated diseases.

作者信息

Liu Huanpeng, Li Huiqi, Yao Xinxin, Yan Xiaoqing, Peng Renyi

机构信息

Institute of Life Sciences & Biomedicine Collaborative Innovation Center of Zhejiang Province, College of Life and Environmental Science, Wenzhou University, Wenzhou, 325035, China.

School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, 325035, China.

出版信息

Environ Pollut. 2025 Oct 1;382:126695. doi: 10.1016/j.envpol.2025.126695. Epub 2025 Jun 21.

DOI:10.1016/j.envpol.2025.126695
PMID:40550382
Abstract

As microplastics (MPs) with smaller particle sizes, nanoplastics (NPs) are widespread in the environment and are characterized by high mobility, a large specific surface area, and a high capacity for adsorption. These properties have made NPs a focal point of global research. NPs have been detected in various biological organisms, including humans, where they can enter cells through biological membranes and even penetrate subcellular structures such as mitochondria and lysosomes, leading to cytotoxicity. This review systematically summarizes the latest research progress of NP-induced mitochondrial damage and its pathophysiological consequences. The key findings revealed that nanoparticles penetrate the biological barrier through endocytosis and membrane fusion, accumulate in the mitochondrial matrix, and trigger cristal deformation, fission fusion imbalance, and membrane depolarization there. Mechanistic studies have shown that NP exposure can disrupt electron transport chain complex activity loss, induce reactive oxygen species (ROS) overproduction, and alter calcium homeostasis. Furthermore, we summarize the various diseases-such as neurodegenerative disorders, diabetes, cardiovascular diseases, and reproductive toxicity-that are linked to NP exposure. Finally, we address the current challenges and future prospects in NP research. This study provides mechanistic insights for the development of mitochondrial targeted therapy strategies and informs regulatory policies regarding exposure thresholds for NPs.

摘要

作为粒径更小的微塑料(MPs),纳米塑料(NPs)在环境中广泛存在,具有高迁移率、大比表面积和高吸附能力等特点。这些特性使纳米塑料成为全球研究的焦点。纳米塑料已在包括人类在内的各种生物体内被检测到,它们可以通过生物膜进入细胞,甚至穿透线粒体和溶酶体等亚细胞结构,从而导致细胞毒性。本综述系统总结了纳米塑料诱导线粒体损伤及其病理生理后果的最新研究进展。关键研究结果表明,纳米颗粒通过内吞作用和膜融合穿透生物屏障,积聚在线粒体基质中,并在那里引发嵴变形、裂变融合失衡和膜去极化。机制研究表明,暴露于纳米塑料会破坏电子传递链复合物活性丧失,诱导活性氧(ROS)过度产生,并改变钙稳态。此外,我们总结了与纳米塑料暴露相关的各种疾病,如神经退行性疾病、糖尿病心血管疾病和生殖毒性。最后,我们阐述了纳米塑料研究当前面临的挑战和未来前景。本研究为线粒体靶向治疗策略的开发提供了机制见解,并为纳米塑料暴露阈值的监管政策提供了参考。

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