1,720,975 research outputs found
Studio della pro-epcidina sierica e dello stato del ferro nella talassemia major ed intermedia
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Terapia combinata con deferxamina e deferiprone nel trattamento delle complicanze cardiache in un paziente affetto da grave emocromatosi giovanile
No full textReversal of hearth failure by deferoxamine and deferiprone combined therapy in a patient affected by severe type juvenile hemochromatosis
No full textHepcidin mutation in a beta-thalassemia major patient with persistent severe iron overload despite chelation therapy
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Hepcidin mutation in a Beta-talassemia major patient with persistent severe iron overload despite chelation therapy
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Mutation analysis of hepcidin and ferroportin genes in Italian prospective blood donors with iron overload
No full textMaintenance of iron balance is essential for humans and requires the coordinate regulation of iron transport into plasma from dietary sources in the duodenum, from recycled senescent red cells in macrophages, and from storage in hepatocytes. Hepcidin, a recently identified antimicrobial peptide produced in the liver, has been shown to play a central role in the homeostatic regulation of iron absorption and distribution [1]. It is a negative regulator of iron absorption in the small intestine and of iron release from macrophages engaged in the recycling of iron senescent erythrocytes [2]. The human hepcidin gene contains three exons that encode a 72-aa precursor (pro-hepcidin) with a characteristic furin cleavage site immediately N-terminal to the 25-aa major hepcidin species found in plasma and urine [3]. Recently, hepcidin has been shown to regulate iron homeostasis by interaction with ferroportin, an iron cellular exporter highly expressed in absorptive enterocytes, macrophages, hepatocytes, and placental cells [4]
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