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Open AccessJournal ArticleDOI

NAD(P)H Oxidase: Role in Cardiovascular Biology and Disease

Kathy K. Griendling, +2 more
- 17 Mar 2000 - 
- Vol. 86, Iss: 5, pp 494-501
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TLDR
Vascular NAD(P)H oxidases have been found to be essential in the physiological response of vascular cells, including growth, migration, and modification of the extracellular matrix and have been linked to hypertension and to pathological states associated with uncontrolled growth and inflammation, such as atherosclerosis.
Abstract
Reactive oxygen species have emerged as important molecules in cardiovascular function. Recent work has shown that NAD(P)H oxidases are major sources of superoxide in vascular cells and myocytes. The biochemical characterization, activation paradigms, structure, and function of this enzyme are now partly understood. Vascular NAD(P)H oxidases share some, but not all, characteristics of the neutrophil enzyme. In response to growth factors and cytokines, they produce superoxide, which is metabolized to hydrogen peroxide, and both of these reactive oxygen species serve as second messengers to activate multiple intracellular signaling pathways. The vascular NAD(P)H oxidases have been found to be essential in the physiological response of vascular cells, including growth, migration, and modification of the extracellular matrix. They have also been linked to hypertension and to pathological states associated with uncontrolled growth and inflammation, such as atherosclerosis.

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TL;DR: There is growing evidence that aging involves, in addition, progressive changes in free radical-mediated regulatory processes that result in altered gene expression.
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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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Increased oxidative stress in obesity and its impact on metabolic syndrome

TL;DR: It is suggested that increased oxidative stress in accumulated fat is an early instigator of metabolic syndrome and that the redox state in adipose tissue is a potentially useful therapeutic target for obesity-associated metabolic syndrome.
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Endothelial Dysfunction in Cardiovascular Diseases: The Role of Oxidant Stress

TL;DR: Accumulating evidence suggests that oxidant stress alters many functions of the endothelium, including modulation of vasomotor tone, and as the role of these various enzyme sources of ROS become clear, it will perhaps be possible to use more specific therapies to prevent their production and ultimately correct endothelial dysfunction.
References
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Journal ArticleDOI

Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells.

TL;DR: The ability of Ang II to stimulate superoxide anion formation is examined and the identity of the oxidases responsible for its production is investigated to suggest that Ang II specifically activates enzyme systems that promote superoxide generation and raise the possibility that these pathways function as second messengers for long-term responses, such as hypertrophy or hyperplasia.
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Requirement for Generation of H2O2 for Platelet-Derived Growth Factor Signal Transduction

TL;DR: The results suggest that H2O2 may act as a signal-transducing molecule, and they suggest a potential mechanism for the cardioprotective effects of antioxidants.
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Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques.

TL;DR: A method is devised which allows the detection and microscopic localization of MMP enzymatic activity directly in tissue sections and may promote destabilization and complication of atherosclerotic plaques and provide novel targets for therapeutic intervention.
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Angiotensin II-mediated hypertension in the rat increases vascular superoxide production via membrane NADH/NADPH oxidase activation. Contribution to alterations of vasomotor tone.

TL;DR: Forms of hypertension associated with elevated circulating levels of angiotensin II may have unique vascular effects not shared by other forms of hypertension because they increase vascular smooth muscle .O2- production via NADH/NADPH oxidase activation.
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Hypercholesterolemia increases endothelial superoxide anion production.

TL;DR: Increased endothelial O2- production in HV may inactivate endothelium-derived nitric oxide and provide a source for other oxygen radicals, contributing to the early atherosclerotic process.
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