Abstract
Oxidative stress represents an imbalance between the production of reactive oxygen species (ROS) and the cellular antioxidant system. Increased levels of oxidative stress contribute to the development of atherosclerosis that eventually leads to thrombosis; a principle cause of heart attacks and strokes. Thrombosis is a consequence of platelet activation and aggregate formation within the circulation. Platelet ROS are mostly generated by reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. NOX2 is an isoform from NADPH oxidase expressed in platelets and an important regulator of platelet activation-associated thrombosis. The present article aims to highlight the relative contribution of NOX2 as a key target of different platelet activation pathways and antiplatelet treatment. (C) 2018 Elsevier Inc. All rights reserved.