A PHD inhibitor prevents changes in the phosphoproteome and capillary rarefaction by CsA: treatment option for CKD?

Gunnar Schley; Margarete Goppelt-Struebe

doi:10.1016/j.kint.2022.06.020

A PHD inhibitor prevents changes in the phosphoproteome and capillary rarefaction by CsA: treatment option for CKD?

Kidney Int. 2022 Oct;102(4):686-688. doi: 10.1016/j.kint.2022.06.020.

Authors

Gunnar Schley¹, Margarete Goppelt-Struebe²

Affiliations

¹ Department of Nephrology and Hypertension, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
² Department of Nephrology and Hypertension, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. Electronic address: [email protected].

PMID: 36150758
DOI: 10.1016/j.kint.2022.06.020

Abstract

Labes et al. analyze the phosphoproteome in a mouse model of chronic cyclosporine A nephrotoxicity and detect significant changes in the angiogenic pathway. Furthermore, they observe reduced hemoglobin levels and capillary rarefaction in the kidney. The authors show that coadministration of the hypoxia-inducible factor prolyl hydroxylase inhibitor daprodustat almost completely prevents changes of the phosphoproteome and capillary rarefaction, suggesting that prolyl hydroxylase domain enzyme inhibitors may preserve microvasculature of the kidney, which is commonly impaired in chronic kidney disease.

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MeSH terms

Animals
Cyclosporine
Hemoglobins
Hypoxia-Inducible Factor-Proline Dioxygenases
Mice
Microvascular Rarefaction*
Prolyl Hydroxylases / metabolism
Prolyl-Hydroxylase Inhibitors* / pharmacology
Prolyl-Hydroxylase Inhibitors* / therapeutic use
Renal Insufficiency, Chronic* / drug therapy

Substances

Hemoglobins
Prolyl-Hydroxylase Inhibitors
Cyclosporine
Prolyl Hydroxylases
Hypoxia-Inducible Factor-Proline Dioxygenases