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2012 ; 1823
(9
): 1434-43
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Hepcidin and iron homeostasis
#MMPMID22306005
Ganz T
; Nemeth E
Biochim Biophys Acta
2012[Sep]; 1823
(9
): 1434-43
PMID22306005
show ga
Despite fluctuations in dietary iron intake and intermittent losses through
bleeding, the plasma iron concentrations in humans remain stable at 10-30 ?M.
While most of the iron entering blood plasma comes from recycling, appropriate
amount of iron is absorbed from the diet to compensate for losses and maintain
nontoxic amounts in stores. Plasma iron concentration and iron distribution are
similarly regulated in laboratory rodents. The hepatic peptide hepcidin was
identified as the systemic iron-regulatory hormone. In the efferent arc, hepcidin
regulates intestinal iron absorption, plasma iron concentrations, and tissue iron
distribution by inducing degradation of its receptor, the cellular iron exporter
ferroportin. Ferroportin exports iron into plasma from absorptive enterocytes,
from macrophages that recycle the iron of senescent erythrocytes, and from
hepatocytes that store iron. In the more complex and less well understood
afferent arc, hepatic hepcidin synthesis is transcriptionally regulated by
extracellular and intracellular iron concentrations through a molecular complex
of bone morphogenetic protein receptors and their iron-specific ligands,
modulators and iron sensors. Through as yet undefined pathways, hepcidin is also
homeostatically regulated by the iron requirements of erythroid precursors for
hemoglobin synthesis. In accordance with the role of hepcidin-mediated iron
redistribution in host defense, hepcidin production is regulated by inflammation
as well. Increased hepcidin concentrations in plasma are pathogenic in
iron-restrictive anemias including anemias associated with inflammation, chronic
kidney disease and some cancers. Hepcidin deficiency causes iron overload in
hereditary hemochromatosis and ineffective erythropoiesis. Hepcidin, ferroportin
and their regulators represent potential targets for the diagnosis and treatment
of iron disorders and anemias. This article is part of a Special Issue entitled:
Cell Biology of Metals.
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