PM2.5 promotes platelet activation and thrombosis via ROS/MAPKs pathway-mediated mitochondrial dysfunction

• Published in: Environmental research Vol. 283; p. 122116
• Main Authors: Xie, Yuquan, Fan, Dongxia, Wu, Biao, Guo, Jianshu, Wang, Ge, Yu, Lu, Zhang, Chihang, Zhao, Jinzhuo, Zhang, Si
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 15.10.2025
• Subjects: mt-COX1; Platelets; PM2.5; ROS; Thrombus; mt-COX1; Platelets; Thrombus; PM2.5; ROS
• ISSN: 0013-9351; 1096-0953; 1096-0953
• DOI: 10.1016/j.envres.2025.122116

Particulate matter (PM2.5) has been identified as a significant risk factor for the development of cardiovascular disease. The current work combined a human panel study with animal experiments intended to investigate the effects of ambient PM2.5 on platelet function and tried to figure out the potential mechanisms. The results showed that inhaling PM2.5 caused platelet aggregation in both human subjects and mouse models, resulting in changes to both the quantity and function of platelets. The multi-omics analysis showed that platelets stimulated by PM2.5 reduce the expression of the mitochondrial complex IV subunit cytochrome c oxidase subunit 1 (mt-COX1). In addition, PM2.5 may lead to an increase in platelet ROS, which activates the mitogen-activated protein kinases (MAPKs) pathway thereby promoting platelet activation and thrombosis. The antioxidant N-acetyl-L-cysteine (NAC) is found to reverse these changes in vitro. In conclusion, the present study provides evidence that exposure to ambient PM2.5 is associated with thrombosis by directly impairing platelet function, in which ROS/MAPKs pathway may be the potential target. •Fine particulate matter (PM2.5) exposure increased platelet reactivity and promoted thrombus formation, with mitochondrial dysfunction.•Reactive oxygen species (ROS) mediate platelet damage caused by PM2.5.•N-acetyl-L-cysteine (NAC) significantly reduced PM2.5-induced platelet aggregation and clot retraction.