title: 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.affiliation: Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA. karin.finberg@duke.edu
authors.forename: Karin E
authors.initials: KE
authors.lastname: Finberg
mesh_terms: D000818:Animals; D005260:Female; D006432:Hemochromatosis / Q000628:therapy*; D008297:Male; D008565:Membrane Proteins / Q000235:genetics*; D012697:Serine Endopeptidases / Q000235:genetics*; D017086:beta-Thalassemia / Q000628:therapy*
chemical_list: D008565:Membrane Proteins; D012697:Serine Endopeptidases; C467801:matriptase 2