M
Marko Bertog
Researcher at University of Erlangen-Nuremberg
Publications - 28
Citations - 1348
Marko Bertog is an academic researcher from University of Erlangen-Nuremberg. The author has contributed to research in topics: Epithelial sodium channel & Aldosterone. The author has an hindex of 18, co-authored 26 publications receiving 1021 citations. Previous affiliations of Marko Bertog include University of Oxford.
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Journal ArticleDOI
Plasmin in Nephrotic Urine Activates the Epithelial Sodium Channel
Per Svenningsen,Claus Bistrup,Ulla G. Friis,Marko Bertog,Silke Haerteis,Bettina Krueger,Jane Stubbe,Ole N. Jensen,Helle C. Thiesson,Torben Rene Uhrenholt,Bente Jespersen,Boye L. Jensen,Christoph Korbmacher,Ole Skøtt +13 more
TL;DR: It is shown that protein-rich urine from nephrotic rats and from patients with nephRotic syndrome activate the epithelial sodium channel (ENaC) in cultured M-1 mouse collecting duct cells and in Xenopus laevis oocytes heterologously expressing ENaC.
Journal ArticleDOI
Targeting zonulin and intestinal epithelial barrier function to prevent onset of arthritis
Narges Tajik,Michael Frech,Oscar Schulz,Fabian Schälter,Sébastien Lucas,Vugar Azizov,Kerstin Dürholz,Franziska Steffen,Yasunori Omata,Andreas Rings,Marko Bertog,Aroldo Rizzo,Aida Iljazovic,Marijana Basic,Arnd Kleyer,Stephan Culemann,Gerhard Krönke,Yubin Luo,Klaus Überla,Udo S. Gaipl,Benjamin Frey,Till Strowig,Kerstin Sarter,Stephan C. Bischoff,Stefan Wirtz,Juan D. Cañete,Francesco Ciccia,Georg Schett,Mario M. Zaiss +28 more
TL;DR: It is shown that both mice and humans with autoimmune arthritis can have dysbiosis and barrier leakiness prior to major signs of inflammatory arthritis, and treatment of mice with a zonulin antagonist can limit collagen-induced arthritis.
Journal ArticleDOI
Aldosterone-dependent and -independent regulation of the epithelial sodium channel (ENaC) in mouse distal nephron.
Viatcheslav Nesterov,Anke Dahlmann,Bettina Krueger,Marko Bertog,Johannes Loffing,Christoph Korbmacher +5 more
TL;DR: It is concluded that ENaC function in the DCT2/CNT is largely independent of ald testosterone which is in contrast to its known aldosterone sensitivity in CNT/CCD.
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HIF-Prolyl Hydroxylases in the Rat Kidney : Physiologic Expression Patterns and Regulation in Acute Kidney Injury
Johannes Schödel,Bernd Klanke,Alexander Weidemann,Björn Buchholz,Wanja Bernhardt,Marko Bertog,Kerstin Amann,Christoph Korbmacher,Michael Wiesener,Christina Warnecke,Armin Kurtz,Kai-Uwe Eckardt,Carsten Willam +12 more
TL;DR: The results implicate the non-uniform expression of HIF-regulating enzymes that modify the hypoxic response in the kidney under both regional and temporal conditions.
Journal ArticleDOI
Additional Disruption of the ClC-2 Cl- Channel Does Not Exacerbate the Cystic Fibrosis Phenotype of Cystic Fibrosis Transmembrane Conductance Regulator Mouse Models *
TL;DR: It is concluded that ClC-2 is unlikely to be a candidate rescue channel in cystic fibrosis, and the data are consistent with a model in which Cl cAMP-activated chloride channel is located in the basolateral membrane.