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Kidney Int. 2020 Apr;97(4):645-647. doi: 10.1016/j.kint.2019.11.036.

Got glycogen? An energy resource in HIF-mediated prevention of ischemic kidney injury.

Author information

1
Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center and Vanderbilt University School of Medicine, Nashville, Tennessee, USA; Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA; Program in Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA. Electronic address: volkerhhaase@gmail.com.

Abstract

Hypoxia-inducible factor activation reprograms glucose metabolism and leads to glycogen accumulation in multiple cell types. In this issue of Kidney International, Ito and colleagues demonstrate that pharmacologic inhibition of hypoxia-inducible factor-prolyl hydroxylase domain oxygen sensors in renal epithelial cells enhances glycogen synthesis and protects from subsequent hypoxia and glucose deprivation. In vivo studies advance the concept that renal glycogen metabolism contributes to cytoprotection afforded by pre-ischemic hypoxia-inducible factor-prolyl hydroxylase domain inhibition.

PMID:
32200856
DOI:
10.1016/j.kint.2019.11.036

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