Oxidative Stress-Induced Endothelial Dysfunction in Cardiovascular Diseases

Cardiovascular disease (CVD) is a major cause of mortality worldwide. A better understanding of the mechanisms underlying CVD is key for better management or prevention. Oxidative stress has been strongly implicated in the pathogenesis of CVD. Indeed, several studies demonstrated that reactive oxygen species (ROS), via different mechanisms, can lead to endothelial cell (EC) dysfunction, a major player in the etiology of several CVDs. ROS appears to modulate a plethora of EC biological processes that are critical for the integrity of the endothelial function. This review seeks to dissect the role of oxidative stress-induced endothelial dysfunction in CVD development, with emphasis on the underlying mechanisms and pathways. Special attention is given to ROS-induced reduction of NO bioavailability, ROS-induced inflammation, and ROS-induced mitochondrial dysfunction. A better understanding and appraisal of these pathways may be essential to attenuate oxidative stress or reverse EC dysfunction, and hence, reduce CVD burden.

Automated summary

Cardiovascular disease is a major cause of global mortality, and oxidative stress plays a crucial role in its pathogenesis. Studies have shown that reactive oxygen species can lead to endothelial dysfunction, contributing to the development of cardiovascular diseases. This review aims to explore the mechanisms underlying oxidative stress-induced endothelial dysfunction in cardiovascular disease, with a focus on the impact of ROS on NO bioavailability, ROS-induced inflammation, and ROS-induced mitochondrial dysfunction.