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Open AccessJournal ArticleDOI

Biochemistry, Physiology, and Pathophysiology of NADPH Oxidases in the Cardiovascular System

Bernard Lassègue, +2 more
- 11 May 2012 - 
- Vol. 110, Iss: 10, pp 1364-1390
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TLDR
The biochemistry of Nox enzymes expressed in the cardiovascular system (Nox1, 2, 4, and 5), their roles in cardiovascular cell biology, and their contributions to disease development are discussed.
Abstract
atherosclerosis, hypertension, cardiac hypertrophy and remodeling, angiogenesis and collateral formation, stroke, and heart failure. In this review, we discuss in detail the biochemistry of Nox enzymes expressed in the cardiovascular system (Nox1, 2, 4, and 5), their roles in cardiovascular cell biology, and their contributions to disease development.

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Citations
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Hydrogen peroxide as a central redox signaling molecule in physiological oxidative stress: Oxidative eustress.

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Role of ROS and RNS Sources in Physiological and Pathological Conditions

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Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology.

TL;DR: It is expected that rigorous translational research of the ANG II signaling pathways including those in large animals and humans will contribute to establishing effective new therapies against various diseases.
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Abstract 1229: Molecular Mechanisms of Angiotensin II-Mediated Mitochondrial Dysfunction: Linking Mitochondrial Oxidative Damage and Vascular Endothelial Dysfunction

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Mitochondrial reactive oxygen species: A double edged sword in ischemia/reperfusion vs preconditioning

TL;DR: Novel therapeutic approaches that selectively target mROS production to reduce postischemic tissue injury may prove efficacious in limiting myocardial dysfunction and infarction and abrogating neurocognitive deficits and neuronal cell death in stroke.
References
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Journal ArticleDOI

The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology

TL;DR: This review summarizes the current state of knowledge of the functions of NOX enzymes in physiology and pathology.
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Oxidation of tetrahydrobiopterin leads to uncoupling of endothelial cell nitric oxide synthase in hypertension

TL;DR: Evidence is obtained that hypertension produces a cascade involving production of ROSs from the NADPH oxidase leading to oxidation of tetrahydrobiopterin and uncoupling of endothelial NO synthase (eNOS), which decreases NO production and increases ROS production from eNOS.
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Role of the T cell in the genesis of angiotensin II–induced hypertension and vascular dysfunction

TL;DR: A previously undefined role for T cells in the genesis of hypertension is identified and a role of inflammation in the basis of this prevalent disease isSupporting a novel therapeutic target for the treatment of high blood pressure.
Journal ArticleDOI

Cell transformation by the superoxide-generating oxidase Mox1

TL;DR: The cloning of mox1 is described, which encodes a homologue of the catalytic subunit of the superoxide-generating NADPH oxidase of phagocytes, gp91phox, which is expressed in colon, prostate, uterus and vascular smooth muscle, but not in peripheral blood leukocytes.
Journal ArticleDOI

Vascular NAD(P)H oxidases: specific features, expression, and regulation

TL;DR: Members of this enzyme family appear to be important in vascular biology and disease and constitute promising targets for future therapeutic interventions.
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