Influence of Vascular Oxidative Stress and Inflammation on the Development and Progression of Atherosclerosis

Cardiovascular disease (CVD) risk factors such as hypertension, diabetes, dyslipidemia, smoking, physical inactivity, and obesity increase production of vascular reactive oxygen species (ROS), which results in a reduction of bioavailable nitric oxide and ultimately endothelial dysfunction and endothelial cell activation. ROS appears to mediate the inflammatory pathways that participate in the development and progression of atherosclerosis. There are numerous markers of oxidative stress and inflammation available for assessing the therapeutic response to interventions, but few are currently recommended for clinical use. Exercise training improves endothelial function via several mechanisms, including increased endothelial nitric oxide synthase—nitric oxide (eNOS-NO)— mediated production, increased activity and amount of antioxidants, attenuated ROS production, and an apparent reduction in systemic inflammation, possibly related to an increase in myokines resulting from skeletal muscle activation. Dietary antioxidant supplementation may improve endothelial function, oxidative stress, and inflammation, but much controversy exists regarding the use of antioxidant supplementation in primary and secondary CVD prevention. The purpose of this article is to review the contribution of vascular oxidative stress and activation of the inflammatory pathways in the pathogenesis of CVD and to review common methods used in clinical research to assess vascular oxidative stress and inflammation in response to therapeutic lifestyle interventions.