Pharmacological inhibition of Vanin-1 is not protective in models of acute and chronic kidney disease.

American Journal of Physiology. Renal Physiology
Kerstin UnterschemmannManuel Grundmann

Abstract

Oxidative stress is a key concept in basic, translational, and clinical research to understand the pathophysiology of various disorders, including cardiovascular and renal diseases. Although attempts to directly reduce oxidative stress with redox-active substances have until now largely failed to prove clinical benefit, indirect approaches to combat oxidative stress enzymatically have gained further attention as potential therapeutic strategies. The pantetheinase Vanin-1 is expressed on kidney proximal tubular cells, and its reaction product cysteamine is described to negatively affect redox homeostasis by inhibiting the replenishment of cellular antioxidative glutathione stores. Vanin-1-deficient mice were shown to be protected against oxidative stress damage. The aim of this study was to elucidate whether pharmacological inhibition of Vanin-1 protects mice from oxidative stress-related acute or chronic kidney injury as well. By studying renal ischemia-reperfusion injury in Col4α3-/- (Alport syndrome) mice and in vitro hypoxia-reoxygenation in human proximal tubular cells we found that treatment with a selective and potent Vanin-1 inhibitor resulted in ample inhibition of enzymatic activity in vitro and in vivo. However, surro...Continue Reading

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Methods Mentioned

BETA
dissection
transfection
Assay
Protein Assay
PCR
biopsies
coronary bypass

Key Resources (RRID) Mentioned

AB_2797508
AB_262011
AB_10015282
SCR_011818
SCR_007165
SCR_002798

Clinical Trials Mentioned

NCT02304666

Software Mentioned

BOXSHADE
Coffee
GraphPad Prism
Image Lab
KinEx

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