PM_2.5 promotes platelet activation and thrombosis via ROS/MAPKs pathway-mediated mitochondrial dysfunction

Area of Science:

• Environmental Health
• Cardiovascular Research
• Hematology

Background:

• Particulate matter (PM_2.5) is a known cardiovascular disease risk factor.
• The specific impact of PM_2.5 on platelet function and underlying mechanisms requires further elucidation.

Purpose of the Study:

• To investigate the effects of ambient PM_2.5 on human and animal platelet function.
• To explore the molecular mechanisms linking PM_2.5 exposure to platelet activation and thrombosis.

Main Methods:

• Combined human panel study and animal experiments.
• Utilized multi-omics analysis to assess platelet changes.
• Investigated the role of reactive oxygen species (ROS) and mitogen-activated protein kinases (MAPKs) pathways.

Main Results:

• PM_2.5 inhalation induced platelet aggregation and altered platelet quantity/function in humans and mice.
• PM_2.5 reduced mt-COX1 expression and increased platelet ROS.
• The ROS/MAPKs pathway was activated, promoting platelet activation and thrombosis.
• N-acetyl-L-cysteine (NAC) reversed PM_2.5-induced changes in vitro.

Conclusions:

• Ambient PM_2.5 exposure is linked to thrombosis through direct impairment of platelet function.
• The ROS/MAPKs pathway is a potential mechanism mediating PM_2.5-induced platelet dysfunction.
• Antioxidant strategies may offer therapeutic potential against PM_2.5-related cardiovascular risks.