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Hepcidin: regulation of the master iron regulator

Iron, an essential nutrient, is required for many diverse biological processes. The absence of a defined pathway to excrete excess iron makes it essential for the body to regulate the amount of iron absorbed; a deficiency could lead to iron deficiency and an excess to iron overload and associated di...

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Detalles Bibliográficos
Autores principales: Rishi, Gautam, Wallace, Daniel F., Subramaniam, V. Nathan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4438303/
https://www.ncbi.nlm.nih.gov/pubmed/26182354
http://dx.doi.org/10.1042/BSR20150014
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author Rishi, Gautam
Wallace, Daniel F.
Subramaniam, V. Nathan
author_facet Rishi, Gautam
Wallace, Daniel F.
Subramaniam, V. Nathan
author_sort Rishi, Gautam
collection PubMed
description Iron, an essential nutrient, is required for many diverse biological processes. The absence of a defined pathway to excrete excess iron makes it essential for the body to regulate the amount of iron absorbed; a deficiency could lead to iron deficiency and an excess to iron overload and associated disorders such as anaemia and haemochromatosis respectively. This regulation is mediated by the iron-regulatory hormone hepcidin. Hepcidin binds to the only known iron export protein, ferroportin (FPN), inducing its internalization and degradation, thus limiting the amount of iron released into the blood. The major factors that are implicated in hepcidin regulation include iron stores, hypoxia, inflammation and erythropoiesis. The present review summarizes our present knowledge about the molecular mechanisms and signalling pathways contributing to hepcidin regulation by these factors.
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spelling pubmed-44383032015-06-01 Hepcidin: regulation of the master iron regulator Rishi, Gautam Wallace, Daniel F. Subramaniam, V. Nathan Biosci Rep Review Article Iron, an essential nutrient, is required for many diverse biological processes. The absence of a defined pathway to excrete excess iron makes it essential for the body to regulate the amount of iron absorbed; a deficiency could lead to iron deficiency and an excess to iron overload and associated disorders such as anaemia and haemochromatosis respectively. This regulation is mediated by the iron-regulatory hormone hepcidin. Hepcidin binds to the only known iron export protein, ferroportin (FPN), inducing its internalization and degradation, thus limiting the amount of iron released into the blood. The major factors that are implicated in hepcidin regulation include iron stores, hypoxia, inflammation and erythropoiesis. The present review summarizes our present knowledge about the molecular mechanisms and signalling pathways contributing to hepcidin regulation by these factors. Portland Press Ltd. 2015-05-19 /pmc/articles/PMC4438303/ /pubmed/26182354 http://dx.doi.org/10.1042/BSR20150014 Text en © 2015 The Author(s) This is an Open Access article distributed under the terms of the Creative Commons Attribution Licence (CC-BY) (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Licence (CC-BY) (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Rishi, Gautam
Wallace, Daniel F.
Subramaniam, V. Nathan
Hepcidin: regulation of the master iron regulator
title Hepcidin: regulation of the master iron regulator
title_full Hepcidin: regulation of the master iron regulator
title_fullStr Hepcidin: regulation of the master iron regulator
title_full_unstemmed Hepcidin: regulation of the master iron regulator
title_short Hepcidin: regulation of the master iron regulator
title_sort hepcidin: regulation of the master iron regulator
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4438303/
https://www.ncbi.nlm.nih.gov/pubmed/26182354
http://dx.doi.org/10.1042/BSR20150014
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