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Regulation of iron homeostasis by the hypoxia-inducible transcription factors (HIFs).
Peyssonnaux C, Zinkernagel AS, Schuepbach RA, Rankin E, Vaulont S, Haase VH, Nizet V, Johnson RS
(2007) J Clin Invest 117: 1926-32
MeSH Terms: Albumins, Animals, Antimicrobial Cationic Peptides, Base Sequence, Cation Transport Proteins, Down-Regulation, Gene Deletion, Hepatocytes, Hepcidins, Homeostasis, Humans, Hypoxia-Inducible Factor 1, Integrases, Iron, Liver, Mice, Mice, Inbred C57BL, Mice, Transgenic, Molecular Sequence Data, Polycythemia, Promoter Regions, Genetic, Protein Binding, Up-Regulation, Von Hippel-Lindau Tumor Suppressor Protein
Show Abstract · Added August 19, 2013
Iron is essential for many biological processes, including oxygen delivery, and its supply is tightly regulated. Hepcidin, a small peptide synthesized in the liver, is a key regulator of iron absorption and homeostasis in mammals. Hepcidin production is increased by iron overload and decreased by anemia and hypoxia; but the molecular mechanisms that govern the hepcidin response to these stimuli are not known. Here we establish that the von Hippel-Lindau/hypoxia-inducible transcription factor (VHL/HIF) pathway is an essential link between iron homeostasis and hepcidin regulation in vivo. Through coordinate downregulation of hepcidin and upregulation of erythropoietin and ferroportin, the VHL-HIF pathway mobilizes iron to support erythrocyte production.
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