CBS 2019
CBSMD教育中心
English

推荐文献

科研文章

荐读文献

Defining Staged Procedures for Percutaneous Coronary Intervention Trials A Guidance Document Robotics in percutaneous cardiovascular interventions Extracorporeal Ultrafiltration for Fluid Overload in Heart Failure: Current Status and Prospects for Further Research Coronary Artery Disease in Patients With Out-of-Hospital Refractory Ventricular Fibrillation Cardiac Arrest Translational Perspective on Epigenetics in Cardiovascular Disease Impact of Oxidative Stress on the Heart and Vasculature: Part 2 of a 3-Part Series Global, regional, and national age-sex specific mortality for 264 causes of death, 1980–2016: a systematic analysis for the Global Burden of Disease Study 2016 Clinical Practice Guideline for Screening and Management of High Blood Pressure in Children and Adolescents Update in the Percutaneous Management of Coronary Chronic Total Occlusions Cardiopulmonary Exercise Testing: What Is its Value?

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.