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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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Transforming growth factor-β-dependent Wnt secretion controls myofibroblast formation and myocardial fibrosis progression in experimental autoimmune myocarditis

TL;DR: TAK1-mediated rapid Wnt protein secretion is identified as a novel downstream key mechanism of TGF-&bgr;-mediated myofibroblast differentiation and myocardial fibrosis progression in human and mouse myocarditis and might represent a promising therapeutic approach against iDCM.
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Obesity Is Associated With Tissue-Specific Activation of Renal Angiotensin-Converting Enzyme In Vivo Evidence for a Regulatory Role of Endothelin

TL;DR: Obesity is associated with the activation of renal ACE in vivo independent of its mRNA expression and enhanced vascular contractility to angiotensin II, providing novel mechanisms by which ET antagonists may exert organ protection.
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Clinical evidence for anti-inflammatory effects of antiplatelet therapy in patients with atherothrombotic disease.

TL;DR: There is substantial evidence that therapy with clopidogrel, a specific antagonist of the platelet P2Y12 ADP-receptor, also leads to reductions in serum levels of CD40 ligand, C-reactive protein, P-selectin, and platelet—leukocyte aggregate formation.
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Endothelial mineralocorticoid receptor activation mediates endothelial dysfunction in diet-induced obesity

TL;DR: Obesity-induced endothelial dysfunction depends on the ‘endothelial’ MR and is mediated by an imbalance of oxidative stress-modulating mechanisms, therefore, MR antagonists may represent an attractive therapeutic strategy in the increasing population of obese patients to decrease vascular dysfunction and subsequent atherosclerotic complications.