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New insights into the links between hypoxia and iron homeostasis.

Authors
  • Renassia, Cyril1, 2, 3, 4
  • Peyssonnaux, Carole1, 2, 3, 4
  • 1 Department Endocrinology Metabolism and Diabetes, INSERM U1016, Institut Cochin.
  • 2 CNRS, UMR8104.
  • 3 Université Paris Descartes, Sorbonne Paris Cité.
  • 4 Laboratory of Excellence GR-Ex, Paris, France. , (France)
Type
Published Article
Journal
Current opinion in hematology
Publication Date
May 01, 2019
Volume
26
Issue
3
Pages
125–130
Identifiers
DOI: 10.1097/MOH.0000000000000494
PMID: 30855332
Source
Medline
Language
English
License
Unknown

Abstract

This review outlines recent discoveries on the crosstalk between oxygen metabolism and iron homeostasis, focusing on the role of HIF-2 (hypoxia inducible factor-2) in the regulation of iron metabolism under physiopathological conditions. The importance of the hepcidin/ferroportin axis in the modulation of intestinal HIF-2 to regulate iron absorption has been recently highlighted. Latest advances also reveal a direct titration of the bone morphogenetic proteins by the erythroferrone contributing to liver hepcidin suppression to increase iron availability. Iron is recycled thanks to erythrophagocytosis of senescent erythrocytes by macrophages. Hemolysis is frequent in sickle cell anemia, leading to increased erythrophagocytosis responsible of the macrophage polarization shift. New findings assessed the effects of hemolysis on macrophage polarization in the tumor microenvironment. Hypoxia signaling links erythropoiesis with iron homeostasis. The use of HIF stabilizing or inhibiting drugs are promising therapeutic approaches in iron-associated diseases.

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