Biochemistry, Physiology, and Pathophysiology of NADPH Oxidases in the Cardiovascular System
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Title
Biochemistry, Physiology, and Pathophysiology of NADPH Oxidases in the Cardiovascular System
Authors
Keywords
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Journal
CIRCULATION RESEARCH
Volume 110, Issue 10, Pages 1364-1390
Publisher
Ovid Technologies (Wolters Kluwer Health)
Online
2012-05-11
DOI
10.1161/circresaha.111.243972
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- Renal Redox-Sensitive Signaling, but Not Blood Pressure, Is Attenuated by Nox1 Knockout in Angiotensin II–Dependent Chronic Hypertension
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- Nox4 Oxidase Overexpression Specifically Decreases Endogenous Nox4 mRNA and Inhibits Angiotensin II–Induced Adventitial Myofibroblast Migration
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- Pioglitazone Inhibits Angiotensin II–Induced Senescence of Endothelial Progenitor Cell
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- Identification of a Conserved Rac-binding Site on NADPH Oxidases Supports a Direct GTPase Regulatory Mechanism
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- Regulation of ROS signal transduction by NADPH oxidase 4 localization
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- Thyroid hormone induces artery smooth muscle cell proliferation: discovery of a new TRα1-Nox1 pathway
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- Expression of NAD(P)H Oxidase Subunits and Their Contribution to Cardiovascular Damage in Aldosterone/Salt-Induced Hypertensive Rat
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- Early increase of Nox4 NADPH oxidase and superoxide generation following endothelin-1-induced stroke in conscious rats
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- Cyclooxygenase 2-Selective and Nonselective Nonsteroidal Anti-Inflammatory Drugs Induce Oxidative Stress by Up-Regulating Vascular NADPH Oxidases
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- Molecular Mechanisms of Angiotensin II–Mediated Mitochondrial Dysfunction
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- Dual Regulation of Cofilin Activity by LIM Kinase and Slingshot-1L Phosphatase Controls Platelet-Derived Growth Factor–Induced Migration of Human Aortic Smooth Muscle Cells
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- Novel redox-dependent regulation of NOX5 by the tyrosine kinase c-Abl
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