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J Am Coll Cardiol. 2017 Jul 11;70(2):212-229. doi: 10.1016/j.jacc.2017.05.035.

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

Author information

1
Center for Cardiology Mainz, Cardiology I, University Medical Center Mainz, Johannes Gutenberg University, Mainz, Germany. Electronic address: tmuenzel@uni-mainz.de.
2
Center for Molecular Cardiology, University of Zurich, Schlieren, Switzerland. Electronic address: giovanni.camici@uzh.ch.
3
Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, Homburg, Germany.
4
Center for Molecular Cardiology, University of Zurich, Schlieren, Switzerland.
5
The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York; Marie-Josée and Henry R. Kravis Cardiovascular Health Center, Icahn School of Medicine at Mount Sinai, New York, New York; Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
6
The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York. Electronic address: jason.kovacic@mountsinai.org.

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.

KEYWORDS:

cardiac; reactive oxygen species; vascular

PMID:
28683969
PMCID:
PMC5663297
DOI:
10.1016/j.jacc.2017.05.035
[Indexed for MEDLINE]
Free PMC Article

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