Hepcidin: regulation of the master iron regulator

Biosci Rep. 2015 Mar 31;35(3):e00192. doi: 10.1042/BSR20150014.

Abstract

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.

Keywords: erythropoiesis; hepcidin; hypoxia; inflammation; iron.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Bone Morphogenetic Proteins / metabolism*
  • Cation Transport Proteins / genetics
  • Cation Transport Proteins / metabolism
  • Cell Hypoxia
  • Erythropoietin / metabolism
  • Hemochromatosis / genetics
  • Hemochromatosis / metabolism
  • Hepcidins / metabolism*
  • Humans
  • Inflammation / metabolism*
  • Iron / metabolism*
  • Mice
  • Signal Transduction
  • Smad Proteins / metabolism*
  • Transferrin / metabolism

Substances

  • Bone Morphogenetic Proteins
  • Cation Transport Proteins
  • Hepcidins
  • Smad Proteins
  • Transferrin
  • metal transporting protein 1
  • Erythropoietin
  • Iron