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Open AccessJournal ArticleDOI

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

TLDR
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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This article is published in Journal of the American College of Cardiology.The article was published on 2017-07-11 and is currently open access. It has received 328 citations till now. The article focuses on the topics: Oxidative stress & Reactive oxygen species.

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Citations
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Journal ArticleDOI

Reactive oxygen species (ROS) as pleiotropic physiological signalling agents.

TL;DR: This work focuses on ROS at physiological levels and their central role in redox signalling via different post-translational modifications, denoted as ‘oxidative eustress’.
Book ChapterDOI

Oxidative Stress: Eustress and Distress in Redox Homeostasis

TL;DR: The global concept of oxidative stress is defined as an imbalance between oxidants and antioxidants in favor of the oxidants, leading to a disruption of redox signaling and control and/or molecular damage as discussed by the authors.
Journal ArticleDOI

Metabolic remodelling in heart failure

TL;DR: It is suggested that the alterations of intermediate substrate metabolism and oxidative stress rather than an ATP deficit per se account for maladaptive cardiac remodelling and dysfunction under resting conditions.
Journal ArticleDOI

Calcium Signaling and Reactive Oxygen Species in Mitochondria

TL;DR: Targeting the dysregulated interplay between excitation–contraction coupling and mitochondrial energetics may ameliorate the progression of heart failure.
Journal ArticleDOI

Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation

TL;DR: The biology of NO and ROS in the cardiovascular system, with special emphasis on their routes of formation and regulation, are presented, as well as the therapeutic challenges and opportunities for the management of no/ROS in cardiovascular disease.
References
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Journal ArticleDOI

Effects of an angiotensin-converting -enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients

TL;DR: Ramipril significantly reduces the rates of death, myocardial infarction, and stroke in a broad range of high-risk patients who are not known to have a low ejection fraction or heart failure.
Journal ArticleDOI

Nitric oxide, superoxide, and peroxynitrite: the good, the bad, and ugly.

TL;DR: The rapid diffusion of nitric oxide between cells allows it to locally integrate the responses of blood vessels to turbulence, modulate synaptic plasticity in neurons, and control the oscillatory behavior of neuronal networks.
Journal ArticleDOI

Oxidative stress and diabetic complications

TL;DR: Athrosclerosis and cardiomyopathy in type 2 diabetes are caused in part by pathway-selective insulin resistance, which increases mitochondrial ROS production from free fatty acids and by inactivation of antiatherosclerosis enzymes by ROS.
Journal ArticleDOI

Role of Oxidative Modifications in Atherosclerosis

TL;DR: An "oxidative response to inflammation" model is proposed as a means of reconciling the response-to-injury and oxidative modification hypotheses of atherosclerosis.
Journal ArticleDOI

Superoxide anion is involved in the breakdown of endothelium-derived vascular relaxing factor

TL;DR: It is demonstrated that EDRF is protected from breakdown by superoxide dismutase (SOD) and Cu2+, but not by catalase, and is inactivated by Fe2+.
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