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Hemodial Int. 2017 Jun;21 Suppl 1:S110-S124. doi: 10.1111/hdi.12567.

HIF-prolyl hydroxylases as therapeutic targets in erythropoiesis and iron metabolism.

Haase VH1,2,3.

Author information

1
Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
2
Departments of Cancer Biology and Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
3
Department of Veterans Affairs Hospital, Medical and Research Services, Tennessee Valley Healthcare System, Nashville, Tennessee, USA.

Abstract

A classic response to systemic hypoxia is the increase in red blood cell production. This response is controlled by the prolyl hydroxylase domain/hypoxia-inducible factor (HIF) pathway, which regulates a broad spectrum of cellular functions. The discovery of this pathway as a key regulator of erythropoiesis has led to the development of small molecules that stimulate the production of endogenous erythropoietin and enhance iron metabolism. This review provides a concise overview of the cellular and molecular mechanisms that govern HIF-induced erythropoietic responses and provides an update on clinical experience with compounds that target HIF-prolyl hydroxylases for anemia therapy.

KEYWORDS:

Anemia; erythropoietin; hypoxia-inducible factor; iron; prolyl hydroxylase

PMID:
28449418
PMCID:
PMC5526677
DOI:
10.1111/hdi.12567
[Indexed for MEDLINE]
Free PMC Article

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