T
Thomas F. Lüscher
Researcher at University of Zurich
Publications - 1613
Citations - 88517
Thomas F. Lüscher is an academic researcher from University of Zurich. The author has contributed to research in topics: Endothelium & Myocardial infarction. The author has an hindex of 134, co-authored 1560 publications receiving 79034 citations. Previous affiliations of Thomas F. Lüscher include University of Texas Southwestern Medical Center & Durham University.
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Journal ArticleDOI
Anti–Tumor Necrosis Factor-α Treatment Improves Endothelial Function in Patients With Rheumatoid Arthritis
David Hürlimann,Adrian Forster,Georg Noll,Frank Enseleit,Rémy Chenevard,Oliver Distler,Markus Béchir,Lukas E. Spieker,Michel Neidhart,Beat A. Michel,Thomas F. Lüscher,Frank Ruschitzka +11 more
TL;DR: The aim of the present study was to assess the effect of chronic antiinflammatory treatment with the anti-TNF-α antibody infliximab on disease activity and endothelial function in patients with active RA.
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Endothelins and endothelin receptor antagonists: therapeutic considerations for a novel class of cardiovascular drugs.
TL;DR: The 21-amino acid peptide endothelin-1 (ET-1) is the predominant isoform of the Endothelin peptide family, which includes ET-2, ET-3, and ET-4 as discussed by the authors.
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Both ETA and ETB receptors mediate contraction to endothelin-1 in human blood vessels.
TL;DR: Vascular smooth muscle cells of human IMA, IMV, and PCA contain both ETA and ETB receptors, whereas the endothelium of IMA andPCA does not express functional ETB receptor linked to nitric oxide and/or prostacyclin production, and inhibition of endothelin-induced contraction in patients requires the use of combined ETA/ETB antagonists.
Journal ArticleDOI
Biology of the endothelium
TL;DR: Risk factors for cardiovascular disease, such as hypertension, hypercholesterolemia, diabetes, vascular aging, and estrogen deficiency, are discussed in terms of their contributions to endothelial dysfunction, which may be the initial step in atherogenesis.
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Mechanisms underlying adverse effects of HDL on eNOS-activating pathways in patients with coronary artery disease
Christian Besler,Kathrin Heinrich,Lucia Rohrer,Carola Doerries,Meliana Riwanto,Diana M. Shih,Angeliki Chroni,Keiko Yonekawa,Sokrates Stein,Nicola Schaefer,Maja Mueller,Alexander Akhmedov,Georgios Daniil,Costantina Manes,Christian Templin,Christophe Wyss,Willibald Maier,Felix C. Tanner,Christian M. Matter,Roberto Corti,Clement E. Furlong,Aldons J. Lusis,Arnold von Eckardstein,Alan M. Fogelman,Thomas F. Lüscher,Ulf Landmesser +25 more
TL;DR: Reduced HDL-associated paraoxonase 1 (PON1) activity is identified as one molecular mechanism leading to the generation of HDL with endothelial PKCβII-activating properties, at least in part due to increased formation of malondialdehyde in HDL.