The DOI matches its Crossref record; 26 of the 27 references it cites were found in a registry or an index.
Iron imports. IV. Hepcidin and regulation of body iron metabolism
Abstract
Hepcidin, a small peptide synthesized in the liver, controls extracellular iron by regulating its intestinal absorption, placental transport, recycling by macrophages, and release from stores. Hepcidin inhibits the cellular efflux of iron by binding to and inducing the degradation of ferroportin, the sole iron exporter in iron-transporting cells. In turn, hepcidin synthesis is increased by iron loading and decreased by anemia and hypoxia. Hepcidin is markedly induced during inflammation, trapping iron in macrophages, decreasing plasma iron concentrations, and contributing to the anemia of inflammation. Hepcidin deficiency due to the dysregulation of its synthesis causes most known forms of hemochromatosis.
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“JunD deficiency induced ROS accumulation in the cells (101).”
From Intracellular iron transport and storage: from molecular mechanisms to health implications (2008) · cites this paper as [101]
Citations
Cites
Hepcidin Regulates Cellular Iron Efflux by Binding to Ferroportin and Inducing Its Internalization
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Self-citationHepcidin, a urinary antimicrobial peptide synthesized in the liver
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Hepcidin, a putative mediator of anemia of inflammation, is a type II acute-phase protein
Nemeth, E., Valore, E. V., Territo, M., Schiller, G., Lichtenstein, A., & Ganz, T. (2003) · Blood · doi:10.1182/blood-2002-10-3235 · Cited by 1,417
Self-citationLEAP-1, a novel highly disulfide-bonded human peptide, exhibits antimicrobial activity
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Hereditary Hemochromatosis — A New Look at an Old Disease
Pietrangelo, A. (2004) · New England Journal of Medicine · doi:10.1056/nejmra031573 · Cited by 992
Mutations in HFE2 cause iron overload in chromosome 1q–linked juvenile hemochromatosis
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Self-citationSevere iron deficiency anemia in transgenic mice expressing liver hepcidin
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Mutant antimicrobial peptide hepcidin is associated with severe juvenile hemochromatosis
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Hepcidin in iron overload disorders
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Self-citationHunter, H. N., Fulton, D. B., Ganz, T., & Vogel, H. J. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m205305200 · Cited by 400
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Constitutive hepcidin expression prevents iron overload in a mouse model of hemochromatosis
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“Moreover, in the mouse model of HFE hemochromatosis, correction of the defect is achieved by overexpression of hepcidin 1 (17).”
Rivera, S., Nemeth, E., Gabayan, V., Lopez, M. A., Farshidi, D., & Ganz, T. (2005) · Blood · doi:10.1182/blood-2005-04-1766 · Cited by 308
Self-citationResistance to hepcidin is conferred by hemochromatosis-associated mutations of ferroportin
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The molecular basis of ferroportin-linked hemochromatosis
De Domenico, I., Ward, D. M., Nemeth, E., Vaughn, M. B., Musci, G., Ganz, T., & Kaplan, J. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0503804102 · Cited by 230
Self-citationThe orchestration of body iron intake: how and where do enterocytes receive their cues?
Frazer, D. M., & Anderson, G. J. (2003) · Blood Cells Molecules and Diseases · doi:10.1016/s1079-9796(03)00039-1 · Cited by 211
Hepcidin excess induces the sequestration of iron and exacerbates tumor-associated anemia
Rivera, S., Liu, L., Nemeth, E., Gabayan, V., Sorensen, O. E., & Ganz, T. (2005) · Blood · doi:10.1182/blood-2004-08-3375 · Cited by 196
Self-citationMechanisms of Iron Accumulation in Hereditary Hemochromatosis
Fleming, R. E., & Sly, W. S. (2002) · Annual Review of Physiology · doi:10.1146/annurev.physiol.64.081501.155838 · Cited by 174
Functional differences between hepcidin 1 and 2 in transgenic mice
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Clinical practice guideline: Red blood cell transfusion in adult trauma and critical care*
Napolitano, L. M., Kurek, S. J., Luchette, F. A., Corwin, H. L., Barie, P. S., Tisherman, S. A., Hébert, P. C., Anderson, G. L., Bard, M. R., Bromberg, W. J., et al. (2009) · Critical Care Medicine · doi:10.1097/ccm.0b013e3181b39f1b · Cited by 560
Metadata
- Authors
- Ganz, T., & Nemeth, E.
- Affiliations
- University of California, Los Angeles (US)
- Venue
- American Journal of Physiology-Gastrointestinal and Liver Physiology
- Publisher
- American Physiological Society
- Published
- 2006-02
- Volume
- 290
- Issue
- 2
- Pages
- G199-G203
- ISSN
- 0193-1857 (ISSN-L)
- 1522-1547
- OpenAlex
- W1978774658
- Cited by
- 347
- References
- 27
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 12 · 2023: 13 · 2022: 8 · 2021: 22 · 2020: 13 · 2019: 10 · 2018: 10 · 2017: 14 · 2016: 13 · 2015: 12 · 2014: 20 · 2013: 18 · 2012: 18
- FWCI
- 21.25
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Gastrointestinal and Liver Physiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Ferroptosis and cancer prognosis
- Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
- Keywords
- hepcidin, iron metabolism, iron imports, ferroportin, intestinal iron absorption, placental iron transport, iron stores, anemia of chronic disease, hypoxia, iron loading, anemia, hemochromatosis, inflammation
- MeSH terms
- Amino Acid Sequence, Anemia, Animals, Hemochromatosis, Humans, Inflammation, Iron, Models, Molecular, Antimicrobial Cationic Peptides, Hepcidins
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