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

By T. Ganz. Blood, 2003

1,569 citations recorded by the source corpus.

Subfields: Genetics, Hematology

View Paper: https://www.semanticscholar.org/paper/c782faa9d78c227f89d4af1ad6dee6bce1a6a7b0

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The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. T. Ganz
2. E. Nemeth
3. V. Haase
4. J. Wish
5. Donat R. Spahn
6. Kostas Pantopoulos
7. S. Rivera
8. D. Richardson

In Hematology

1. T. Ganz
2. E. Nemeth
3. V. Haase
4. Donat R. Spahn
5. J. Wish
6. Kostas Pantopoulos
7. G. Papanikolaou
8. S. Rivera

Citations in the corpus

• Iron metabolism and toxicity. (2005, background): “Recently, a dual function compatible with both a bstoresQ and berythropoieticQ regulator has been proposed for hepcidin, a small circulating peptide derived from the liver (Ganz, 2003).”
• Aptamers in the Therapeutics and Diagnostics Pipelines (2018, background): “Hepcidin is a small peptide that is the key regulator of iron hemostasis [55].”
• IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin. (2004, positive): “In a model that we proposed (12, 34) as an extension of earlier hypotheses (13, 35), IL-6–stimulated increase in plasma hepcidin concentration blocks the release of iron from macrophages that recycle iron from senescent erythrocytes.”
• Mutations in HFE2 cause iron overload in chromosome 1q–linked juvenile hemochromatosis (2004, background): “, whose levels correlate inversely with rates of iron uptake in the gut and with the release of iron from macrophage”
• Assessing iron status: beyond serum ferritin and transferrin saturation. (2006, background): “Hepcidin activity in normal individuals is increased in the setting of inflammation/infection, primarily through the release of IL-6 by Kupffer cells in the liver (15).”
• Regulation of erythropoiesis by hypoxia-inducible factors (2013, background): “Chronically elevated serum hepcidin levels are frequently associated with inflammatory states (interleukin-6 induces hepcidin transcription via JAK/STAT signaling) and lead to reduced ferroportin surface expression and hypoferremia, lending support to the notion that hepcidin has a key role in the p”
• Anemia and Patient Blood Management in Hip and Knee Surgery: A Systematic Review of the Literature (2010, background): “By inducing the internalization of ferroportin in enteric cells and macrophages, the presence of high serum levels of hepcidin plays a key role in the development of anemia of chronic inflammation by impairing the absorption of orally administrated iron and by leading to iron sequestration in macrop”
• The changing faces of glutathione, a cellular protagonist. (2003, background): “…repeated hemorrhage and chronic inflammation concomitant with continued parenchymal cell death, result in iron overload in the corresponding locations (Ganz, 2003), leading to oxidative damage through the Fenton reaction (Minotti and Aust, 1989; Miller et al., 1990; Halliwell and Gutteridge, 2007).”
• The Evolution of Iron Chelators for the Treatment of Iron Overload Disease and Cancer (2005, background): “It is thought that hepcidin negatively regulates intestinal iron absorption, maternal-fetal iron transport across the placenta, and iron release from hepatic stores and macrophages (Ganz, 2003).”