Reactive Oxygen Species (ROS) and oxidised low-density lipoprotein (oxLDL) play diverse roles in platelet function and may lead to maladaptive platelet phenotypes in disease states.
Blood platelets are anucleate cells that play a vital role in haemostasis, innate immunity, angiogenesis, and wound healing. However, the inappropriate activation of platelets also contributes to vascular inflammation, atherogenesis, and thrombosis. Platelet activation is a highly complex receptor-mediated process that involves a multitude of signalling intermediates in which Reactive Oxygen Species (ROS) are proposed to play an important role. However, like for many cells, changes in the balance of ROS generation and/or scavenging in disease states may lead to the adoption of maladaptive platelet phenotypes. Here, we review the diverse roles of ROS in platelet function and how ROS are linked to specific platelet activation pathways. We also examine how changes in disease, particularly the plasma oxidised low-density lipoprotein (oxLDL), affect platelet ROS generation and platelet function.
Cheah et al. (Thu,) conducted a review in Platelet activation, vascular inflammation, atherogenesis, and thrombosis. Reactive Oxygen Species (ROS) and oxidised low-density lipoprotein (oxLDL) was evaluated. Reactive Oxygen Species (ROS) and oxidised low-density lipoprotein (oxLDL) play diverse roles in platelet function and may lead to maladaptive platelet phenotypes in disease states.