“…Evidence for oxidative stress-driven thrombosis is derived from multiple independent studies using targeted interruption of genes involved in oxidant regulation [51][52][53], pharmacologic inhibition of oxidant sources [54,55], chemical degraders or generators of oxidants [56,57], cellular assays that involve oxidants (e.g., platelet activation and endothelial cell-mediated procoagulant activity) [58][59][60], and animal models of thrombosis [57,61]. We focus on atherothrombosis, which is arterial thrombosis in the context of atherosclerosis, based on evidence from our lab and others that oxidative stress is prominent in dyslipidemia and other chronic atherogenic states and that redox cues in these settings are converted to a pro-thrombotic response [2,62,63].…”