Hepcidin-ferroportin axis in health and disease

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

81 Scopus citations

Abstract

Hepcidin is central to regulation of iron metabolism. Its effect on a cellular level involves binding ferroportin, the main iron export protein, resulting in its internalization and degradation and leading to iron sequestration within ferroportin-expressing cells. Aberrantly increased hepcidin leads to systemic iron deficiency and/or iron restricted erythropoiesis. Furthermore, insufficiently elevated hepcidin occurs in multiple diseases associated with iron overload. Abnormal iron metabolism as a consequence of hepcidin dysregulation is an underlying factor resulting in pathophysiology of multiple diseases and several agents aimed at manipulating this pathway have been designed, with some already in clinical trials. In this chapter, we present an overview of and rationale for exploring the development of hepcidin agonists and antagonists in various clinical scenarios.

Original languageEnglish
Title of host publicationIron Metabolism
Subtitle of host publicationHepcidin
EditorsGerald Litwack
PublisherAcademic Press Inc.
Pages17-45
Number of pages29
ISBN (Print)9780128178423
DOIs
StatePublished - 1 Jan 2019

Publication series

NameVitamins and Hormones
Volume110
ISSN (Print)0083-6729

Keywords

  • Anemia of inflammation
  • Erythroferrone
  • Hepcidin antagonists
  • Hepcidin mimetics
  • Hepcidin:ferroportin axis
  • Hereditary hemochromatosis
  • Iron metabolism
  • Polycythemia vera
  • β-thalassemia

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