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Nikos Werner

Researcher at University of Bonn

Publications -  139
Citations -  9630

Nikos Werner is an academic researcher from University of Bonn. The author has contributed to research in topics: Medicine & Endothelium. The author has an hindex of 38, co-authored 114 publications receiving 8381 citations. Previous affiliations of Nikos Werner include Saarland University & Humboldt University of Berlin.

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Circulating endothelial progenitor cells and cardiovascular outcomes.

TL;DR: The association between baseline levels of endothelial progenitor cells and death from cardiovascular causes, the occurrence of a first major cardiovascular event, revascularization, hospitalization, anddeath from all causes were evaluated.
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Physical Training Increases Endothelial Progenitor Cells, Inhibits Neointima Formation, and Enhances Angiogenesis

TL;DR: Physical activity increases the production and circulating numbers of EPCs via a partially NO-dependent, antiapoptotic effect that could potentially underlie exercise-related beneficial effects on cardiovascular diseases.
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Intravenous Transfusion of Endothelial Progenitor Cells Reduces Neointima Formation After Vascular Injury

TL;DR: Systemically applied spleen‐derived MNCs and EPCs home to the site of vascular injury, resulting in an enhanced reendothelialization associated with decreased neointima formation and novel insights in stem cell biology are allowed.
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Estrogen Increases Bone Marrow–Derived Endothelial Progenitor Cell Production and Diminishes Neointima Formation

TL;DR: Estrogens increase numbers of EPCs by antiapoptotic effects leading to accelerated vascular repair and decreased neointima formation in mice and human women with increased estrogen plasma concentrations.
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Bone Marrow–Derived Progenitor Cells Modulate Vascular Reendothelialization and Neointimal Formation: Effect of 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibition

TL;DR: Vascular lesion development initiated by endothelial cell damage is moderated by bone marrow–derived progenitor cells, and 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibition promotes bone marrow-dependent reendothelialization and diminishes vascular lesionDevelopment.