REVIEW

Molecular pathogenesis of iron overload

D Trinder¹, C Fox², G Vautier³ and J K Olynyk⁴

¹ Department of Medicine and Western Australian Institute for Medical Research, University of Western Australia, Australia
² Department of Gastroenterology, Fremantle Hospital, Fremantle, Western Australia, Australia
³ Department of Gastroenterology, Fremantle Hospital, Fremantle, Western Australia, Australia, and Royal Defence Medical College, Gosport, UK
⁴ Department of Medicine and Western Australian Institute for Medical Research, University of Western Australia, Australia, and Department of Gastroenterology, Fremantle Hospital, Fremantle, Western Australia, Australia

Correspondence to:
Correspondence to:
Associate Professor J Olynyk, University Department of Medicine, PO Box 480, Fremantle 6959, Western Australia, Australia;
jolynyk{at}cyllene.uwa.edu.au

Our current understanding of iron absorption under normal conditions is presented, together with an overview of the clinical disorders of iron overload and the molecular processes that contribute to increased iron deposition in iron overload. Recently, a number of new genes involved in iron metabolism have been identified which is allowing the molecular mechanisms of iron absorption to be elucidated.

Keywords: divalent metal transporter 1; ferroportin; iron regulating elements; haemochromatosis; haephestin; hepcidin; iron

Abbreviations: DMT1, divalent metal transporter 1; HFE, haemochromatosis protein; HH, hereditary haemochromatosis; IRE, iron regulatory element; IRP, iron regulatory protein; NTBI, non-transferrin bound iron; TBI, transferrin bound iron; TfR1, transferrin receptor 1; TfR2, transferrin receptor 2

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