Iron homeostasis: insights from genetics and animal models

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Abstract
Iron balance must be strictly maintained to ensure that adequate amounts of iron are available for vital functions and to avoid the toxicity that results from iron excess. Disorders of iron deficiency and iron overload develop when iron balance is disrupted. Iron is absorbed by enterocytes in the proximal intestine; it is stored in hepatocytes, used primarily by erythroid cells, and is recycled by specialized macrophages. There are similarities in the iron-transport strategies used by these different cell types, but tissue-specific differences also exist. Two iron transporters, DMT1 (an importer) and ferroportin1 (an exporter — also known as Ireg1 or MTP1), have been identified by positional cloning. Targeted mutagenesis has produced new mouse models of human iron disorders, including models for hereditary haemochromatosis and aceruloplasminaemia. Despite recent advances in our understanding of iron absorption and iron recycling, many mechanistic details remain to be understood.
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