Cysteine and methionine oxidation in thrombotic disorders

Thrombosis is the leading cause of death in many diseased conditions. Oxidative stress is characteristic of these condi-tions. Yet, the mechanisms through which oxidants become prothrombotic are unclear. Recent evidence suggests protein cysteine and methionine oxidation as prothrombotic regulators. These oxidative post-translational modifications occur on pro-teins that participate in the thrombotic process, including Src family kinases, protein disulfide isomerase, 02 glycoprotein I, von Willebrand factor, and fibrinogen. New chemical tools to identify oxidized cysteine and methionine proteins in throm-bosis and hemostasis, including carbon nucleophiles for cysteine sulfenylation and oxaziridines for methionine, are critical to understanding why clots occur during oxidative stress. These mechanisms will identify alternative or novel therapeutic approaches to treat thrombotic disorders in diseased conditions.

Automated summary

Thrombosis is the main cause of death in many diseases, but the mechanisms through which oxidants become prothrombotic are not clear. Protein cysteine and methionine oxidation have been found to be regulators of thrombosis. New chemical tools are needed to identify oxidized cysteine and methionine proteins in thrombosis and hemostasis, in order to understand why clots occur during oxidative stress and develop alternative therapeutic approaches for thrombotic disorders.