Accumulation of reactive oxygen species (ROS) can induce both protein tyrosine nitration and endothelial dysfunction in atherosclerosis. Endothelial dysfunction refers to impaired endothelium-dependent vasorelaxation that can be triggered by an imbalance in nitric oxide (NO) production and consumption. ROS reacts with NO to generate peroxynitrite, decreasing NO bioavailability. Peroxynitrite also promotes protein tyrosine nitration in vivo that can affect protein structure and function and further damage endothelial function. In this review, we discuss the process of protein tyrosine nitration, increased expression of nitrated proteins in cardiovascular disease and their association with endothelial dysfunction, and the interference of tyrosine nitration with antioxidants and the protective role in endothelial dysfunction. These may lead us to the conception that protein tyrosine nitration may be one of the causes of endothelial dysfunction, and help us gain information about the mechanism of endothelial dysfunction underlying atherosclerosis.
Keywords: Atherosclerosis; Cardiovascular disease; Endothelial dysfunction; Protein tyrosine nitration; ROS/RNS.
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