Therapeutic targeting of the HIF oxygen-sensing pathway: Lessons learned from clinical studies

被引：44
作者：
Haase, Volker H. [1 ,2 ,3 ]
机构：
[1] Vanderbilt Univ, Med Ctr, Dept Med, Nashville, TN USA
[2] Vanderbilt Univ, Sch Med, Dept Canc Biol, Nashville, TN 37212 USA
[3] Vanderbilt Univ, Sch Med, Dept Mol Physiol & Biophys, Nashville, TN 37212 USA
来源：
EXPERIMENTAL CELL RESEARCH | 2017年 / 356卷 / 02期
关键词：
Hypoxia; Hypoxia-inducible factor; Anemia; Prolyl hydroxylase domain; Chronic kidney disease; Clinical trials; Oxygen; PROLYL HYDROXYLASE INHIBITOR; CHRONIC KIDNEY-DISEASE; INDUCIBLE FACTOR-I; PULMONARY-ARTERY PRESSURE; ROXADUSTAT FG-4592; EPOETIN-ALPHA; TRANSCRIPTIONAL ACTIVATION; ERYTHROPOIETIN PRODUCTION; IRON-DEFICIENCY; REGULATES HEPCIDIN;
D O I：
10.1016/j.yexcr.2017.05.004
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
The oxygen-sensitive hypoxia-inducible factor (HIF) pathway plays a central role in the control of erythropoiesis and iron metabolism. The discovery of prolyl hydroxylase domain (PHD) proteins as key regulators of HIF activity has led to the development of inhibitory compounds that are now in phase 3 clinical development for the treatment of renal anemia, a condition that is commonly found in patients with advanced chronic kidney disease. This review provides a concise overview of clinical effects associated with pharmacologic PHD inhibition and was written in memory of Professor Lorenz Poellinger.
引用
收藏
页码：160 / 165
页数：6
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