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Hypoxia-inducible factor activation in diabetic kidney disease.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology. (Fredrik Palm)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology. (Fredrik Palm)
(English)In: Current opinion in nephrology and hypertension, ISSN 1062-4821, E-ISSN 1473-6543Article, review/survey (Refereed) Epub ahead of print
Abstract [en]

PURPOSE OF REVIEW:

Tissue hypoxia is present in kidneys from diabetic patients and constitutes a central pathway to diabetic kidney disease (DKD). This review summarizes regulation of hypoxia inducible factor (HIF) and interventions towards the same for treatment of DKD.

RECENT FINDINGS:

In the hypoxic diabetic kidney, HIF activity and the effects of HIF signaling seem to be cell-specific. In mesangial cells, elevated glucose levels induce HIF activity by a hypoxia-independent mechanism. Elevated HIF activity in glomerular cells promotes glomerulosclerosis and albuminuria, and inhibition of HIF protects glomerular integrity. However, tubular HIF activity is suppressed and HIF activation protects mitochondrial function and prevents development of diabetes-induced tissue hypoxia, tubulointerstitial fibrosis and proteinuria. No clinical treatment targeting kidney hypoxia is currently available, but development of prolyl hydroxylase inhibitors to promote HIF activity to treat renal anemia could potentially also target diabetes-induced kidney hypoxia.

SUMMARY:

Increasing HIF activity in the diabetic kidney may possess a novel target for treatment of DKD by improving kidney oxygen homeostasis. However, HIF-mediated glomerulosclerosis may be a concern. The kidney outcomes from the ongoing clinical trials using prolyl hydroxylase inhibitors may provide additional insights into the complex role of HIF signaling in the diabetic kidney.

Keyword [en]
diabetes, hypoxia inducible factor-1 a, hypoxia inducible factor-1 b, nephropathy, prolyl-hydroxylase
National Category
Physiology
Research subject
Physiology
Identifiers
URN: urn:nbn:se:uu:diva-322784DOI: 10.1097/MNH.0000000000000341OAI: oai:DiVA.org:uu-322784DiVA: diva2:1103500
Funder
Swedish Research CouncilSwedish Diabetes AssociationSwedish Society for Medical Research (SSMF)
Available from: 2017-05-30 Created: 2017-05-30 Last updated: 2017-05-30

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CiteExportLink to record
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  • apa
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