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Victor Rizzo

Researcher at Temple University

Publications -  69
Citations -  4019

Victor Rizzo is an academic researcher from Temple University. The author has contributed to research in topics: Caveolae & Endothelium. The author has an hindex of 31, co-authored 65 publications receiving 3270 citations. Previous affiliations of Victor Rizzo include Beth Israel Deaconess Medical Center & Albany Medical College.

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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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In Situ Flow Activates Endothelial Nitric Oxide Synthase in Luminal Caveolae of Endothelium with Rapid Caveolin Dissociation and Calmodulin Association

TL;DR: Data demonstrate a physiological relevant mechanotransduction event directly in caveolae at the luminal endothelial cell surface to release eNOS from its inhibitory association with caveolin, apparently to allow more complete activation by calmodulin and other possible effectors.
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Recruitment of endothelial caveolae into mechanotransduction pathways by flow conditioning in vitro.

TL;DR: It is reported that chronic exposure to shear stress alters caveolin expression and distribution, increases caveolae density, and leads to enhanced mechanosensitivity to subsequent changes in hemodynamic forces within cultured endothelial cells.
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Rapid Mechanotransduction in Situ at the Luminal Cell Surface of Vascular Endothelium and Its Caveolae

TL;DR: It is shown, for the first time, that not only does mechanotransduction occur at the endothelial cell surface directly exposed to vascular flow in vivo but also increased flowin situ induces rapid tyrosine phosphorylation of luminal endothelialcell surface proteins located primarily in the plasmalemmal invaginations called caveolae.
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Shear-induced endothelial NOS activation and remodeling via heparan sulfate, glypican-1, and syndecan-1

TL;DR: It is demonstrated how EC can transform fluid shear forces into diverse biomolecular and biomechanical responses, with GPC1 acting as a centralized mechanotransmission agent and SDC1 functioning in decentralized mechanotranmission.