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New insights into the regulation of iron homeostasis.
Eur J Clin Invest. 2006 May; 36(5):301-9.EJ

Abstract

Hepcidin evolves as a potent hepatocyte-derived regulator of the body's iron distribution piloting the flow of iron via, and directly binding, to the cellular iron exporter ferroportin. The hepcidin-ferroportin axis dominates the iron egress from all cellular compartments that are critical to iron homeostasis, namely placental syncytiotrophoblasts, duodenal enterocytes, hepatocytes and macrophages of the reticuloendothelial system. The gene that encodes hepcidin expression (HAMP) is subject to regulation by proinflammatory cytokines, such as IL-6 and IL-1; excessive hepcidin production explains the relative deficiency of iron during inflammatory states, eventually resulting in the anaemia of inflammation. The haemochromatosis genes HFE, TfR2 and HJV potentially facilitate the transcription of HAMP. Disruption of each of the four genes leads to a diminished hepatic release of hepcidin consistent with both a dominant role of hepcidin in hereditary haemochromatosis and an upstream regulatory role of HFE, TfR2 and HJV on HAMP expression. The engineered generation of hepcidin agonists, mimetics or antagonists could largely broaden current therapeutic strategies to redirect the flow of iron.

Authors+Show Affiliations

Department of Medicine III, Medical University of Vienna, Vienna, Austria.No affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

16634833

Citation

Deicher, R, and W H. Hörl. "New Insights Into the Regulation of Iron Homeostasis." European Journal of Clinical Investigation, vol. 36, no. 5, 2006, pp. 301-9.
Deicher R, Hörl WH. New insights into the regulation of iron homeostasis. Eur J Clin Invest. 2006;36(5):301-9.
Deicher, R., & Hörl, W. H. (2006). New insights into the regulation of iron homeostasis. European Journal of Clinical Investigation, 36(5), 301-9.
Deicher R, Hörl WH. New Insights Into the Regulation of Iron Homeostasis. Eur J Clin Invest. 2006;36(5):301-9. PubMed PMID: 16634833.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - New insights into the regulation of iron homeostasis. AU - Deicher,R, AU - Hörl,W H, PY - 2006/4/26/pubmed PY - 2006/9/16/medline PY - 2006/4/26/entrez SP - 301 EP - 9 JF - European journal of clinical investigation JO - Eur J Clin Invest VL - 36 IS - 5 N2 - Hepcidin evolves as a potent hepatocyte-derived regulator of the body's iron distribution piloting the flow of iron via, and directly binding, to the cellular iron exporter ferroportin. The hepcidin-ferroportin axis dominates the iron egress from all cellular compartments that are critical to iron homeostasis, namely placental syncytiotrophoblasts, duodenal enterocytes, hepatocytes and macrophages of the reticuloendothelial system. The gene that encodes hepcidin expression (HAMP) is subject to regulation by proinflammatory cytokines, such as IL-6 and IL-1; excessive hepcidin production explains the relative deficiency of iron during inflammatory states, eventually resulting in the anaemia of inflammation. The haemochromatosis genes HFE, TfR2 and HJV potentially facilitate the transcription of HAMP. Disruption of each of the four genes leads to a diminished hepatic release of hepcidin consistent with both a dominant role of hepcidin in hereditary haemochromatosis and an upstream regulatory role of HFE, TfR2 and HJV on HAMP expression. The engineered generation of hepcidin agonists, mimetics or antagonists could largely broaden current therapeutic strategies to redirect the flow of iron. SN - 0014-2972 UR - https://www.unboundmedicine.com/medline/citation/16634833/New_insights_into_the_regulation_of_iron_homeostasis_ L2 - https://doi.org/10.1111/j.1365-2362.2006.01633.x DB - PRIME DP - Unbound Medicine ER -