Hepcidin, a key regulator of iron metabolism and mediator of anemia of inflammation.

@article{Ganz2003HepcidinAK,
  title={Hepcidin, a key regulator of iron metabolism and mediator of anemia of inflammation.},
  author={Tomas Ganz},
  journal={Blood},
  year={2003},
  volume={102 3},
  pages={
          783-8
        }
}
  • T. Ganz
  • Published 1 August 2003
  • Biology, Medicine
  • Blood
Human hepcidin, a 25-amino acid peptide made by hepatocytes, may be a new mediator of innate immunity and the long-sought iron-regulatory hormone. The synthesis of hepcidin is greatly stimulated by inflammation or by iron overload. Evidence from transgenic mouse models indicates that hepcidin is the predominant negative regulator of iron absorption in the small intestine, iron transport across the placenta, and iron release from macrophages. The key role of hepcidin is confirmed by the presence… 
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Hepcidin: a direct link between iron metabolism and immunity.
  • D. Vyoral, J. Petrak
  • Biology, Medicine
    The international journal of biochemistry & cell biology
  • 2005
Hepcidin, originally discovered in urine as a bactericidal peptide synthesized by hepatocytes was later proved to be a key regulator of iron metabolism at the whole body level, namely, in conditions…
Deregulation of proteins involved in iron metabolism in hepcidin-deficient mice.
TLDR
The level of iron-related proteins was analyzed by Western blot and immunohistochemistry in hepcidin-deficient mice, a mouse model of severe hemochromatosis, and it was hypothesized that the deregulation of these proteins might be central in the pathogenesis of iron overload, providing key therapeutic targets for iron disorders.
New insights into the regulation of iron homeostasis
TLDR
The engineered generation of hepcidin agonists, mimetics or antagonists could largely broaden current therapeutic strategies to redirect the flow of iron.
[The role of hepcidin in iron metabolism in inflammatory bowel diseases].
TLDR
The discovery of the biological properties of hepcidin clarified the relationship between iron homeostasis, immune response, and anaemia of chronic disease and there are data that antihePCidin treatment may be an effective treatment of anaemia in inflammatory bowel disease.
Hepcidin, an overview of biochemical and clinical properties
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The current review highlights the significant role of hepcidin in the iron homeostasis and as an antimicrobial agent.
Anemia of inflammation: the hepcidin link
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Increasingly, experiments suggest the hepatocyte is not just the iron storage depot but is the ‘command central’ for the maintenance of iron homeostasis.
Suppression of iron-regulatory hepcidin by vitamin D.
TLDR
Data show that vitamin D is a potent regulator of the hepcidin-ferroportin axis in humans and highlight a potential new strategy for the management of anemia in patients with low vitamin D and/or CKD.
Role of the hepcidin-ferroportin axis in pathogen-mediated intracellular iron sequestration in human phagocytic cells.
TLDR
This is the first study in which TLR1-9-mediated iron homeostasis in human macrophages was evaluated, and the outcome of this study elucidates the mechanism of iron dysregulation in macrophage during infection.
Hepcidin: A key regulator of iron.
TLDR
Hapcidin is the central regulator of iron homeostasis in the body and its role is quite inevitable in understanding metastasis in certain cancers and its pathological roles in blood and iron diseases could lead to new therapies.
Kupffer cells modulate iron homeostasis in mice via regulation of hepcidin expression
TLDR
The data suggest that Kupffer cells control body iron homeostasis by exerting negative regulatory signals toward hepcidin expression, which may be primarily referred to the secretion of yet unidentified hePCidin-suppressing molecules by K upffer cells.
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References

SHOWING 1-10 OF 51 REFERENCES
Hepcidin, a putative mediator of anemia of inflammation, is a type II acute-phase protein.
TLDR
The linkage of hepcidin induction to inflammation in humans supports its proposed role as a key mediator of anemia of inflammation.
The gene encoding the iron regulatory peptide hepcidin is regulated by anemia, hypoxia, and inflammation.
TLDR
Modifications of hepcidin gene expression suggest a key role for hepciridin in iron homeostasis under various pathophysiological conditions, which may support the pharmaceutical use of hePCidin agonists and antagonists in various ironHomeostasis disorders.
Hepcidin: A putative iron-regulatory hormone relevant to hereditary hemochromatosis and the anemia of chronic disease
  • R. Fleming, W. Sly
  • Biology, Medicine
    Proceedings of the National Academy of Sciences of the United States of America
  • 2001
TLDR
The paper by Nicolas et al. in this issue of PNAS presents the exciting possibility that a central player in the communication of body iron stores to the intestinal absorptive cells may have been identified, the hepatic protein hepcidin.
Inappropriate expression of hepcidin is associated with iron refractory anemia: implications for the anemia of chronic disease.
TLDR
It is concluded that hepcidin plays a major, causative role in the anemia observed in the subgroup of patients with hepatic adenomas, and it is speculated that it is important in the pathogenesis of theAnemia of chronic disease in general.
Lack of hepcidin gene expression and severe tissue iron overload in upstream stimulatory factor 2 (USF2) knockout mice
TLDR
A peculiar phenotype of Usf2−/− mice that progressively develop multivisceral iron overload is reported; plasma iron overcomes transferrin binding capacity, and nontransferrin-bound iron accumulates in various tissues including pancreas and heart.
Disrupted hepcidin regulation in HFE-associated haemochromatosis and the liver as a regulator of body iron homoeostasis
TLDR
Lack of HAMP upregulation in HFE-associated haemochromatosis despite significant hepatic iron loading indicates that HFE plays an important part in the regulation of hepcidin expression in response to iron overload, and the increase in hepatic IREG1 expression in haemolife suggests that IREG2 could function to facilitate the removal of excess iron from the liver.
Hepcidin expression inversely correlates with the expression of duodenal iron transporters and iron absorption in rats.
TLDR
Both hepcidin expression and iron absorption can be regulated before iron stores and erythropoiesis are affected, and transferrin saturation may signal such changes.
Iron, infections, and anemia of inflammation.
  • R. Jurado
  • Biology, Medicine
    Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
  • 1997
TLDR
Understanding the molecular basis of iron withholding by the human host, both in the absence of and during infection, and that of iron acquisition by microorganisms may provide us with new and innovative antimicrobial agents and vaccines.
C/EBPα Regulates Hepatic Transcription of Hepcidin, an Antimicrobial Peptide and Regulator of Iron Metabolism
TLDR
During rat liver development, amounts of Hepcidin transcripts were very low in fetal liver, strongly and transiently increased shortly after birth, and reappeared in adult liver, demonstrating that C/EBPα is likely to be a key regulator of HEPC gene transcription and provide a novel mechanism for cross-talk between the C/ EBP pathway and iron metabolism.
Targeted gene disruption reveals an essential role for ceruloplasmin in cellular iron efflux.
TLDR
An essential physiologic role for ceruloplasmin is revealed in determining the rate of iron efflux from cells with mobilizable iron stores, suggesting that iron accumulation results from altered compartmentalization within the iron cycle.
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