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

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.

Keywords: Diseases; Mitochondrial dysfunction; NPs; Programmed cell death.