Impact of Oxidative Stress on the Heart and Vasculature

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 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 arrhythmias, 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 anti-oxidant systems that orchestrate region-specific ROS production and removal. ROS 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 via direct and irreversible oxidative damage to macromolecules, as well as disruption of redox-dependent vascular wall signaling processes.

Schisandrin C targets Keap1 and attenuates oxidative stress by activating Nrf2 pathway in Ang II‐challenged vascular endothelium

“…Oxidative stress has been linked to the onset of various cardiovascular complications, particularly in hypertension (Forstermann et al, 2017;McSweeney et al, 2016;Munzel et al, 2017). Ang II infusion induces aberrant ROS production in the aorta, resulting in dysfunction of the endothelium (Dikalov et al, 2014).…”

“…Extensive cellular and molecular studies have identified putative mediators, which include increased oxidative stress, inflammation, mitochondrial dysfunction, and endothelial cell (EC) apoptosis (Hou et al, ; Kroller‐Schon et al, ; Vaka et al, ), that participate in the progression of endothelial dysfunction. Among these various functional events, oxidative stress seems to be upstream of the cascade (Forstermann, Xia, & Li, ; McSweeney, Warabi, & Siow, ; Munzel et al, ).…”

Cannabinoids, the Heart of the Matter

“…Oxidative stress is a common factor across all contributing pathologies in CVD 21. Oxidative stress arises when the production of reactive oxygen species exceeds the total antioxidant capacity of the body.…”

Progenitor Cell Dysfunction: The Role of Endothelial Precursors in Heart Failure

“…Moreover, it has noted that there is possibility to change of endothelial cell immune phenotype to cardiac cell phenotype in animal model [22]. Whether similar effects trigger structure and functional abnormality in cell precursors that involve in the pathogenesis of HF is not well established, although accumulation of reactive oxygen species leading to the swelling and fragmentation of mitochondria of EPCs has now described as factor of decreased repair ability of precursors [23]. Indeed, enhancement of oxidative stress and mitochondrial dysfunction of EPCs may negatively effect of number and function of ones (mobbing, proliferation, regeneration, apoptosis, differentiation, cell-cell interaction, survival) through intracellular signaling pathways (Akt/nitric oxide, PI3K/nitric oxide), which may operate in signal-regulated kinase and the inflammatory genes expression, such as interleukin-6 and TNF-α, and synthesis of specific miRNAs (-126, -128, -130) [24,25].…”