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Journal ArticleDOI

Disorders of iron metabolism.

Nancy C. Andrews
- 23 Dec 1999 - 
- Vol. 341, Iss: 26, pp 1986-1995
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TLDR
Iron has the capacity to accept and donate electrons readily, interconverting between ferric (Fe2+) and ferrous (Fe3+) forms, which makes it a useful component of cytochromes, oxygen-binding molecules, and many enzymes.
Abstract
Iron has the capacity to accept and donate electrons readily, interconverting between ferric (Fe2+) and ferrous (Fe3+) forms. This capability makes it a useful component of cytochromes, oxygen-bind...

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Citations
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Journal ArticleDOI

IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin

TL;DR: These studies in human liver cell cultures, mice, and human volunteers indicate that IL-6 is the necessary and sufficient cytokine for the induction of hepcidin during inflammation and that the IL- 6-hepcid in axis is responsible for the hypoferremia of inflammation.
Journal ArticleDOI

Hepcidin, a key regulator of iron metabolism and mediator of anemia of inflammation.

TL;DR: Human hepcidin, a 25-amino acid peptide made by hepatocytes, may be a new mediator of innate immunity and the long-sought iron-regulatory hormone and its role in iron metabolism could lead to new therapies for hemochromatosis and anemia of inflammation.
Journal ArticleDOI

Targeted Drug Delivery via the Transferrin Receptor-Mediated Endocytosis Pathway

TL;DR: The OX26 monoclonal antibody against the rat transferrin receptor offers great promise in the delivery of therapeutic agents across the blood-brain barrier to the brain and serves as a potential alternative to viral vector for gene therapy.
Journal ArticleDOI

Hepcidin and iron homeostasis.

TL;DR: Hepcidin, ferroportin and their regulators represent potential targets for the diagnosis and treatment of iron disorders and anemias.
References
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Journal ArticleDOI

The hereditary hemochromatosis protein, HFE, specifically regulates transferrin-mediated iron uptake in HeLa cells.

TL;DR: It is shown that the expression of HFE reduces 55Fe uptake from Tf by 33% but does not affect the endocytic or exocytic rates of TfR cycling, which has implications for the understanding of cellular iron homeostasis in organs such as the liver, pancreas, heart and spleen.
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Two novel missense mutations of the HFE gene (I105T and G93R) and identification of the S65C mutation in Alabama hemochromatosis probands.

TL;DR: It is concluded that uncommon HFE exon and intron mutations may be discovered among hemochromatosis patients who have "atypical" HFE genotypes.
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A Family of Congenital Atransferrinemia

TL;DR: An 8-yr-old boy with familial congenital atransferrinemia was studied and it appeared that the hemopoiesis was stimulated by transferrin and that the clinical effectiveness of transferrin was related to the resultant increased red cell production and the duration of the effect to the life-span of the erythrocyte.
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Use of desferrioxamine in the treatment of aceruloplasminemia

TL;DR: Treatment for 10 months with the iron chelator desferrioxamine decreased brain iron stores, prevented progression of the neurological symptoms, and reduced plasma lipid peroxidation suggest that early treatment with this chelator may be useful in patients to diminish central nervous system iron accumulation and to prevent or ameliorate neurological symptoms associated with neurodegeneration.
Journal ArticleDOI

Associations of iron overload in Africa with hepatocellular carcinoma and tuberculosis: Strachan's 1929 thesis revisited

TL;DR: It is suggested that iron overload in black Africans may be a risk factor for death from hepatocellular carcinoma and fordeath from tuberculosis.
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