Key result
Reactive oxygen species and oxidized lipids drive pathological platelet hyperactivity in cardiovascular disease.
Why the study?
Changes in ROS generation or scavenging in disease states may lead to maladaptive platelet phenotypes, but how ROS and oxidized lipids link to specific platelet activation pathways warrants review.
This review highlights the critical role of reactive oxygen species and oxidized lipids in modulating platelet activation and promoting atherothrombosis, identifying potential future therapeutic targets.
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.
No takes yet. Share an insight, caveat, or question.
Cheah et al. (2025) conducted a review in Cardiovascular disease and thrombosis. Reactive Oxygen Species (ROS) was evaluated. Reactive oxygen species mediate specific platelet activation pathways, and their dysregulation by oxidized lipids drives maladaptive platelet hyperactivity in cardiovascular diseases.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: