Polystyrene microplastics induce pulmonary fibrosis by promoting alveolar epithelial cell ferroptosis through cGAS/STING signaling

Autor: Jinming Zhang, Jiangzhou Du, Dongyu Liu, Jinzhong Zhuo, Lanhe Chu, Yanqun Li, Lin Gao, Mingming Xu, Weimou Chen, Wufeng Huang, Lingyan Xie, Junwei Chen, Xiaojing Meng, Fei Zou, Shaoxi Cai, Hangming Dong
Jazyk: angličtina
Rok vydání: 2024
Předmět:
Zdroj: Ecotoxicology and Environmental Safety, Vol 277, Iss , Pp 116357- (2024)
Druh dokumentu: article
ISSN: 0147-6513
DOI: 10.1016/j.ecoenv.2024.116357
Popis: Polystyrene microplastics (PS-MPs) are new types of environmental pollutant that have garnered significant attention in recent years since they were found to cause damage to the human respiratory system when they are inhaled. The pulmonary fibrosis is one of the serious consequences of PS-MPs inhalation. However, the impact and underlying mechanisms of PS-MPs on pulmonary fibrosis are not clear. In this study, we studied the potential lung toxicity and PS-MPs-developed pulmonary fibrosis by long-term intranasal inhalation of PS-MPs. The results showed that after exposing to the PS-MPs, the lungs of model mouse had different levels of damage and fibrosis. Meanwhile, exposing to the PS-MPs resulted in a markedly decrease in glutathione (GSH), an increase in malondialdehyde (MDA), and iron overload in the lung tissue of mice and alveolar epithelial cells (AECs). These findings suggested the occurrence of PS-MP-induced ferroptosis. Inhibitor of ferroptosis (Fer-1) had alleviated the PS-MPs-induced ferroptosis. Mechanically, PS-MPs triggered cell ferroptosis and promoted the development of pulmonary fibrosis via activating the cGAS/STING signaling pathway. Inhibition of cGAS/STING with G150/H151 attenuated pulmonary fibrosis after PS-MPs exposure. Together, these data provided novel mechanistic insights of PS-MPs-induced pulmonary fibrosis and a potential therapeutic paradigm.
Databáze: Directory of Open Access Journals