Striking the target in iron overload disorders
Karin E. Finberg
Karin E. Finberg
Published March 25, 2013
Citation Information: J Clin Invest. 2013;123(4):1424-1427. https://doi.org/10.1172/JCI68889.
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Commentary

Striking the target in iron overload disorders

Abstract

The liver, a major site of body iron stores, mediates key responses that preserve systemic iron homeostasis. In this issue of the JCI, Guo et al. demonstrate that administration of antisense oligonucleotides that reduce expression of Tmprss6, a hepatic protein that plays an essential role in maintaining iron balance, can attenuate disease severity in mouse models of human iron overload disorders. These data reveal the potential of novel TMPRSS6-targeted therapies for the treatment of clinical conditions such as hereditary hemochromatosis and β-thalassemia.

Authors

Karin E. Finberg

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Figure 1

Effect of hepcidin on iron transport in the duodenum and in macrophages.

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Effect of hepcidin on iron transport in the duodenum and in macrophages....
(Left) After dietary iron is taken up by duodenal enterocytes, ferroportin mediates iron export across the basolateral membrane into the plasma. (Right) After red blood cells are phagocytosed by macrophages, hemoglobin-derived iron is exported by ferroportin into the plasma. In both of these cell types, hepcidin limits iron export by triggering the internalization and degradation of ferroportin in lysosomes.