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Carlos F. Sánchez-Ferrer

Researcher at Autonomous University of Madrid

Publications -  108
Citations -  4146

Carlos F. Sánchez-Ferrer is an academic researcher from Autonomous University of Madrid. The author has contributed to research in topics: Endothelium & Vascular smooth muscle. The author has an hindex of 33, co-authored 101 publications receiving 3662 citations. Previous affiliations of Carlos F. Sánchez-Ferrer include Hospital Universitario La Paz.

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G-protein-coupled receptor Mas is a physiological antagonist of the angiotensin II type 1 receptor

TL;DR: It is demonstrated that Mas can hetero-oligomerize with the AT1 receptor and by so doing inhibit the actions of angiotensin II, a novel demonstration that a G-protein–coupled receptor acts as a physiological antagonist of a previously characterized receptor.
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Endothelial dysfunction in aged humans is related with oxidative stress and vascular inflammation.

TL;DR: It is concluded that the age‐dependent endothelial dysfunction in human vessels is due to the combined effect of oxidative stress and vascular wall inflammation.
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Mechanisms involved in the aging-induced vascular dysfunction.

TL;DR: Prevention or reversion of those mechanisms leading to endothelial dysfunction through life style modifications or pharmacological interventions could markedly improve cardiovascular health in older people.
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Extracellular PBEF/NAMPT/visfatin activates pro-inflammatory signalling in human vascular smooth muscle cells through nicotinamide phosphoribosyltransferase activity

TL;DR: Through its intrinsic NAMPT activity, ePBEF/NAMPT/visfatin appears to be a direct contributor to vascular inflammation, a key feature of atherothrombotic diseases linked to metabolic disorders.
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Visfatin/Nampt: an adipokine with cardiovascular impact

TL;DR: Visfatin/Nampt effects on cytokine and chemokine secretion, macrophage survival, leukocyte recruitment by endothelial cells, vascular smooth muscle inflammation and plaque destabilization make of this adipokine an active factor in the development and progression of atherosclerosis.