[Advances in research on the mechanisms of reactive oxygen species in platelet activation and thrombosis].

Platelets play a crucial role in atherosclerosis and thrombus formation, and their activation is regulated by reactive oxygen species (ROS). ROS in platelets primarily originates from nicotinamide adenine dinucleotide phosphate oxidase (NOX). Upon activation of glycoprotein Ⅵ (GPⅥ), ROS generation can be induced through both spleen tyrosine kinase (Syk) -dependent and Syk-independent pathways. In addition, the protease-activated receptor (PAR) signaling pathway not only activates NOX, but our latest research has revealed that it can also induce mitochondria-dependent ROS generation independently of GPⅥ. This finding expands the redox signaling pathways regulated by PAR and suggests mitochondria as a potential novel target for antithrombotic interventions. Endogenous ROS participate in the cascade of platelet activation and thrombus stabilization by modifying key signaling proteins and regulating ion channel function. Therefore, targeting ROS generation pathways associated with GPⅥ/PAR holds promise for developing precise therapeutic strategies for thrombotic diseases. This review summarizes the underlying mechanisms and provides a theoretical basis for the prevention and treatment of conditions such as atherosclerosis.