Key result
Oxidative stress drives vascular disease and heart failure via direct damage and impaired redox signaling.
Why the study?
Oxidative stress is a key pathological mechanism shared by many causes of cardiac and vascular disease, impacting heart failure and vascular dysfunction.
This review highlights the central pathological role of oxidative stress and reactive oxygen species in the development and progression of heart failure and vascular disease.
Targeting oxidative stress remains theoretical for cardiovascular management; leaves open whether modulating these.
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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Münzel et al. (2017) conducted a review in Vascular disease and heart failure. Oxidative stress was evaluated. Excessive oxidative stress and reactive oxygen species promote vascular disease and heart failure through direct oxidative damage and disruption of redox-dependent signaling processes.
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