Andrea Janessa
Tuebingen, BW 72076, Germany
Last Updated: 09/26/2026
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Found 10 publications
Impact of aldosterone deficiency on the development of diuretic resistance in mice.
Journal: Pflugers Archiv : European journal of physiology
Published: December 23, 2024
Sodium retention in nephrotic syndrome is independent of the activation of the membrane-anchored serine protease prostasin (CAP1/PRSS8) and its enzymatic activity.
Journal: Pflugers Archiv : European journal of physiology
Published: January 26, 2022
Proteolytic activation of the epithelial sodium channel (ENaC) by factor VII activating protease (FSAP) and its relevance for sodium retention in nephrotic mice.
Journal: Pflugers Archiv : European journal of physiology
Published: August 26, 2021
Experimental nephrotic syndrome leads to proteolytic activation of the epithelial Na+ channel in the mouse kidney.
Journal: American journal of physiology. Renal physiology
Published: August 23, 2021
Essential role of DNA-PKcs and plasminogen for the development of doxorubicin-induced glomerular injury in mice.
Journal: Disease models & mechanisms
Published: March 24, 2021
Renal effects of the serine protease inhibitor aprotinin in healthy conscious mice.
Journal: Acta pharmacologica Sinica
Published: December 10, 2020
Plasminogen deficiency does not prevent sodium retention in a genetic mouse model of experimental nephrotic syndrome.
Journal: Acta physiologica (Oxford, England)
Published: February 29, 2020
Urokinase-type plasminogen activator (uPA) is not essential for epithelial sodium channel (ENaC)-mediated sodium retention in experimental nephrotic syndrome.
Journal: Acta physiologica (Oxford, England)
Published: February 27, 2019
Plasma kallikrein activates the epithelial sodium channel in vitro but is not essential for volume retention in nephrotic mice.
Journal: Acta physiologica (Oxford, England)
Published: December 24, 2017
Showing 1-10 of 10
Last Updated: 09/26/2026