Oxidative Stress, Endothelial Dysfunction and Atherosclerosis

Abstract

This review focuses on the role of oxidative processes in atherosclerosis and the cardiovascular diseases (CVD) that can arise as a result. Atherosclerosis represents a state of heightened oxidative stress characterized by lipid and protein oxidation in the vascular wall. Overproduction of reactive oxygen species (ROS) under pathophysiologic conditions forms an integral part of the development of CVD, and in particular atherosclerosis. Endothelial dysfunction, characterized by a loss of nitric oxide (NO) bioactivity, occurs early on in the development of atherosclerosis, and determines future vascular complications. Although the molecular mechanisms responsible for mitochondria-mediated disease processes are not clear, oxidative stress seems to play an important role. In general, ROS are essential to the functions of cells, but adequate levels of antioxidant defenses are required in order to avoid the harmful effects of excessive ROS production. In this review, we will provide a summary of the cellular metabolism of reactive oxygen species (ROS) and its role in pathophysiological processes such as atherosclerosis; and currently available antioxidants and possible reasons for their efficacy and inefficacy in ameliorating oxidative stress-mediated diseases.

Acetylation‐dependent regulation of mitochondrial ALDH2 activation by SIRT3 mediates acute ethanol‐induced eNOS activation

“…Previous studies suggest that low dose of ethanol can induce eNOS activation [3][4][5], which contributes to ethanol protective effects on the cardiovascular system. Our results confirmed these findings that ethanol treatment (20-35 mM) could elicit rapid eNOS phosphorylation and activation (<5 min) by activating PI3K/Akt pathway in HAECs.…”

“…In addition, ethanol, as a small exogenous liposoluble molecule, can be metabolized by mitochondrial enzyme systems, accompanied by reactive oxygen species (ROS) generation. ROS have detrimental or beneficial effects on eNOS activation depending on its concentrations [5,6]. During ethanol exposure, ROS level is dependent on the capability of antioxidant systems to antagonize ROS generation.…”

Endothelial dysfunction in rat adjuvant‐induced arthritis: Up‐regulation of the vascular arginase pathway

“…The presence of chronic inflammation is responsible for the development of subclinical atherosclerosis and increased incidence of cardiovascular events in arthritis patients (4). It is well established that endothelial dysfunction is the most important step in early atherogenesis and also contributes to the development of clinical features in the later stages of vascular disease, including progression of atherosclerotic plaque (5,6). In addition, endothelial dysfunction is a predictor of cardiovascular events in the general population (7).…”

The Hemostatic System in Arterial Thrombosis and Coronary Atherosclerosis

“…In a healthy environment, there is a balanced expression of these products which maintains the integrity of the luminal surface, ensuring protection of the vessel wall and providing a healthy blood flow. Endothelial damage upsets this balance to initiate events that play a pivotal role in the progression of the atherosclerotic process 3 . Changes in endothelial structure and function, provoked by pathophysiological stimuli, can result IJBR (2013) 04 (09) www.ssjournals.com in alterations in the interactions of endothelium with the cellular and macromolecular components of circulating blood and of the blood vessel wall.…”

“…The protective mechanisms include the non-thrombogenic properties of intact endothelial cells, fluid-phase anti-proteases, and the dissolution of fibrin by the fibrinolytic system. Thrombogenic stimuli include injury or loss of endothelial cells and activation of platelets and blood coagulation 3 .…”