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David S. Weber

Researcher at Emory University

Publications -  20
Citations -  2480

David S. Weber is an academic researcher from Emory University. The author has contributed to research in topics: Vascular smooth muscle & Lung injury. The author has an hindex of 13, co-authored 20 publications receiving 2360 citations.

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Journal ArticleDOI

Angiotensin II stimulation of NAD(P)H oxidase activity: upstream mediators.

TL;DR: The results suggest that c-Src, EGF receptor transactivation, phosphatidylinositol-3-kinase, and Rac play important roles in the sustained Ang II–mediated activation of vascular smooth muscle cell NAD(P)H oxidases and provide insight into the integrated signaling mechanisms whereby Ang II stimulation leads to activation of the growth-related NAD( P)H oxidationases.
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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.
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Transient Receptor Potential Vanilloid 4–Mediated Disruption of the Alveolar Septal Barrier A Novel Mechanism of Acute Lung Injury

TL;DR: In this paper, vanilloid transient receptor potential channel (TRPV4) activation was found to disrupt the alveolar septal barrier, leading to acute lung injury and hypoxemia.
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TRPV4 initiates the acute calcium-dependent permeability increase during ventilator-induced lung injury in isolated mouse lungs

TL;DR: It is concluded that rapid calcium entry through TRPV4 channels is a major determinant of the acute vascular permeability increase in lungs following high PIP ventilation.
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Phosphoinositide-dependent kinase 1 and p21-activated protein kinase mediate reactive oxygen species-dependent regulation of platelet-derived growth factor-induced smooth muscle cell migration.

TL;DR: Data indicate that PDGF-induced VSMC migration is ROS dependent and identify the Src/PDK1/PAK1 signaling pathway as an important ROS-sensitive mediator of migration.