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

Thomas Münzel, Giovanni G. Camici, Christoph Maack, Nicole R. Bonetti, Valentin Fuster, Jason C. Kovacic

Research output: Contribution to journalReview articlepeer-review

344 Citations (Scopus)

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.
Original languageEnglish
Pages (from-to)212-229
Number of pages18
JournalJournal of the American College of Cardiology
Volume70
Issue number2
DOIs
Publication statusPublished - 11 Jul 2017
Externally publishedYes

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