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World J Gastroenterol. Sep 21, 2007; 13(35): 4725-4736
Published online Sep 21, 2007. doi: 10.3748/wjg.v13.i35.4725
Liver iron transport
Ross M Graham, Anita CG Chua, Carly E Herbison, John K Olynyk, Debbie Trinder
Ross M Graham, Anita CG Chua, Carly E Herbison, John K Olynyk, Debbie Trinder, School of Medicine and Pharmacology, Fremantle Hospital, University of Western Australia, Fremantle, Western Australia, Australia
John K Olynyk, Debbie Trinder, Western Australian Institute for Medical Research, Nedlands, Western Australia, Australia
Author contributions: All authors contributed equally to the work.
Supported by The National Health and Medical Research Council of Australia
Correspondence to: Dr. Debbie Trinder, School of Medicine and Pharmacology, Fremantle Hospital, University of Western Australia, PO Box 480, Fremantle, 6959, Western Australia, Australia. dtrinder@cyllene.uwa.edu.au
Telephone: +618-9431-3640 Fax: +618-9431-2977
Received: March 30, 2007
Revised: April 10, 2007
Accepted: April 14, 2007
Published online: September 21, 2007
Abstract

The liver plays a central role in iron metabolism. It is the major storage site for iron and also expresses a complex range of molecules which are involved in iron transport and regulation of iron homeostasis. An increasing number of genes associated with hepatic iron transport or regulation have been identified. These include transferrin receptors (TFR1 and 2), a ferrireductase (STEAP3), the transporters divalent metal transporter-1 (DMT1) and ferroportin (FPN) as well as the haemochromatosis protein, HFE and haemojuvelin (HJV), which are signalling molecules. Many of these genes also participate in iron regulatory pathways which focus on the hepatic peptide hepcidin. However, we are still only beginning to understand the complex interactions between liver iron transport and iron homeostasis. This review outlines our current knowledge of molecules of iron metabolism and their roles in iron transport and regulation of iron homeostasis.

Keywords: Liver; Iron homeostasis; Iron uptake; Iron release; Iron transporters; Hereditary haemochromatosis