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W. Robert Taylor

Researcher at Emory University

Publications -  44
Citations -  7206

W. Robert Taylor is an academic researcher from Emory University. The author has contributed to research in topics: Angiotensin II & Vascular smooth muscle. The author has an hindex of 27, co-authored 44 publications receiving 6794 citations. Previous affiliations of W. Robert Taylor include United States Department of Veterans Affairs & Veterans Health Administration.

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Superoxide Production and Expression of Nox Family Proteins in Human Atherosclerosis

TL;DR: Several Nox proteins, including gp91phox and Nox4, may contribute to increased intracellular oxidative stress in human coronary atherosclerosis in a cell-specific manner and thus may be involved in the genesis and progression of human coronary Atherosclerotic disease.
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Role of NADH/NADPH Oxidase–Derived H2O2 in Angiotensin II–Induced Vascular Hypertrophy

TL;DR: Data indicate that AT1 receptor-mediated production of superoxide generated by the NADH/NADPH oxidase is followed by an increase in intracellular H2O2, suggesting a specific role for these oxygen species and scavenging systems in modifying the intrACEllular redox state in vascular growth.
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p22phox mRNA Expression and NADPH Oxidase Activity Are Increased in Aortas From Hypertensive Rats

TL;DR: The findings suggest that Ang II-induced hypertension activates the NADPH/NADH oxidase system by upregulating mRNA levels of one or several components of this oxid enzyme system, including the p22phox, and that the NAD PH/NadH oxidases system is associated with the pathology of hypertension in vivo.
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In vivo imaging of hydrogen peroxide with chemiluminescent nanoparticles

TL;DR: It is demonstrated that nanoparticles formulated from peroxalate esters and fluorescent dyes can image hydrogen peroxide in vivo with high specificity and sensitivity and deep-tissue-imaging capability.
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Nox1 overexpression potentiates angiotensin ii-induced hypertension and vascular smooth muscle hypertrophy in transgenic mice

TL;DR: Data indicate that smooth muscle-specific Nox1 overexpression augments the oxidative, pressor, and hypertrophic responses to Ang II, supporting the concept that medial Nox 1 participates in the development of cardiovascular pathologies.