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Impact of Oxidative Stress on the Heart and Vasculature: Part 2 of a 3-Part Series Screening for Cardiovascular Disease Risk With Electrocardiography: US Preventive Services Task Force Recommendation Statement Association of All-Cause and Cardiovascular Mortality With High Levels of Physical Activity and Concurrent Coronary Artery Calcification Healthy Behavior, Risk Factor Control, and Survival in the COURAGE Trial Comparison of the Efficacy and Safety Outcomes of Edoxaban in 8040 Women Versus 13 065 Men With Atrial Fibrillation in the ENGAGE AF-TIMI 48 Trial Optical frequency-domain imaging findings to predict good stent expansion after rotational atherectomy for severely calcified coronary lesions Is Cardiac Diastolic Dysfunction a Part of Post-Menopausal Syndrome? Diagnostic Accuracy of Angiography-Based Quantitative Flow Ratio Measurements for Online Assessment of Coronary Stenosis
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Review Article2017 Jul 11;70(2):212-229.

JOURNAL：J Am Coll Cardiol. Article Link

Impact of Oxidative Stress on the Heart and Vasculature: Part 2 of a 3-Part Series

Münzel T, Camici GG, Kovacic JC et al. Keywords: cardiac; reactive oxygen species; vascular

ABSTRACT

Vascular disease and heart failure impart an enormous burden in terms of global morbidity and mortality. Although there are many different causes of cardiac and vascular disease, most causes share an important pathological mechanism: oxidative stress. In the failing heart, oxidative stress occurs in the myocardium and correlates with left ventricular dysfunction. Reactive oxygen species (ROS) negatively affect myocardial calcium handling, cause arrhythmia, and contribute to cardiac remodeling by inducing hypertrophic signaling, apoptosis, and necrosis. Similarly, oxidative balance in the vasculature is tightly regulated by a wealth of pro- and antioxidant systems that orchestrate region-specific ROS production and removal. Reactive oxygen species also regulate multiple vascular cell functions, including endothelial and smooth muscle cell growth, proliferation, and migration; angiogenesis; apoptosis; vascular tone; host defenses; and genomic stability. However, excessive levels of ROS promote vascular disease through direct and irreversible oxidative damage to macromolecules, as well as disruption of redox-dependent vascular wall signaling processes.

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