J
Jakob Voelkl
Researcher at Johannes Kepler University of Linz
Publications - 95
Citations - 2984
Jakob Voelkl is an academic researcher from Johannes Kepler University of Linz. The author has contributed to research in topics: Calcification & Vascular smooth muscle. The author has an hindex of 28, co-authored 89 publications receiving 2289 citations. Previous affiliations of Jakob Voelkl include Charité & University of Tübingen.
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Journal ArticleDOI
High salt reduces the activation of IL-4– and IL-13–stimulated macrophages
Katrina J. Binger,Matthias Gebhardt,Matthias Heinig,Carola Rintisch,Agnes Schroeder,Wolfgang Neuhofer,Karl F. Hilgers,Arndt Manzel,Christian Schwartz,Markus Kleinewietfeld,Jakob Voelkl,Valentin Schatz,Ralf A. Linker,Florian Lang,David Voehringer,Mark D. Wright,Norbert Hubner,Ralf Dechend,Jonathan Jantsch,Jens Titze,Dominik N. Müller +20 more
TL;DR: Evidence is provided that high salt reduces noninflammatory innate immune cell activation and may thus lead to an overall imbalance in immune homeostasis, and a mechanism by which NaCl inhibits full M2 macrophage activation is identified.
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Spironolactone ameliorates PIT1-dependent vascular osteoinduction in klotho-hypomorphic mice
Jakob Voelkl,Ioana Alesutan,Christina Leibrock,Leticia Quintanilla-Martinez,Volker Kuhn,Martina Feger,Sobuj Mia,Mohamed Siyabeldin E. Ahmed,Kevin P. Rosenblatt,Makoto Kuro-o,Florian Lang +10 more
TL;DR: It is shown that the mineralocorticoid receptor antagonist spironolactone reduced vascular and soft tissue calcification and increased the life span of kl/kl mice, without significant effects on 1,25(OH)2D3, FGF23, calcium, and phosphate plasma concentrations.
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Sgk1-Dependent Stimulation of Cardiac Na+/H+ Exchanger Nhe1 by Dexamethasone
Jakob Voelkl,Venkanna Pasham,Mohamed Siyabeldin E. Ahmed,Britta Walker,Kalina Szteyn,Dietmar Kuhl,Bernhard Metzler,Ioana Alesutan,Florian Lang +8 more
TL;DR: Sgk1 is critically involved in the phosphorylation and activation of the cardiac Na+/H+ exchanger Nhe1, and the effects of dexamethasone were significantly blunted in sgK1-/- mice.
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The Uremic Toxin Acrolein Promotes Suicidal Erythrocyte Death
TL;DR: Whether the uremic toxin acrolein could trigger eryptosis is explored, an effect at least in part due to stimulation of ceramide formation with subsequent sensitisation of the erythrocytes to cytosolic Ca2+.
Journal ArticleDOI
Stimulation of suicidal erythrocyte death by increased extracellular phosphate concentrations.
Jakob Voelkl,Kousi Alzoubi,Abdel-Karim Mamar,Mohamed Siyabeldin E. Ahmed,Majed Abed,Florian Lang +5 more
TL;DR: It is hypothesized that suicidal erythrocyte death is triggered by complexed CaHPO4, an effect depending on extracellular but not intracellular Ca2+ concentration.