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Integrin A5B1-mediated endocytosis of polystyrene nanoplastics: Implications for human lung disease and therapeutic targets
Summary
This study identified a specific protein, integrin alpha-5-beta-1, as a key gateway that allows polystyrene nanoplastics to enter human lung cells. Once inside, the nanoplastics triggered inflammation, oxidative stress, and cell damage that could contribute to respiratory disease and lung cancer risk. The discovery of this entry mechanism could provide a potential drug target for reducing the harmful effects of inhaled nanoplastics on lung health.
The extensive use of plastic products has exacerbated micro/nanoplastic (MPs/NPs) pollution in the atmosphere, increasing the incidence of respiratory diseases and lung cancer. This study investigates the uptake and cytotoxicity mechanisms of polystyrene (PS) NPs in human lung epithelial cells. Transcriptional analysis revealed significant changes in cell adhesion pathways following PS-NPs exposure. Integrin α5β1-mediated endocytosis was identified as a key promoter of PS-NPs entry into lung epithelial cells. Overexpression of integrin α5β1 enhanced PS-NPs internalization, exacerbating mitochondrial Ca2+ dysfunction and depolarization, which induced reactive oxygen species (ROS) production. Mitochondrial dysfunction triggered by PS-NPs led to oxidative damage, inflammation, DNA damage, and necrosis, contributing to lung diseases. This study elucidates the molecular mechanism by which integrin α5β1 facilitates PS-NPs internalization and enhances its cytotoxicity, offering new insights into potential therapeutic targets for microplastic-induced lung diseases.