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The gene encoding the iron regulatory peptide hepcidin is regulated by anemia, hypoxia, and inflammation
Open accessAbstract
The present study was aimed at determining whether hepcidin, a recently identified peptide involved in iron metabolism, plays a role in conditions associated with both iron overload and iron deficiency.Hepcidin mRNA levels were assessed in two models of anemia, acute hemolysis provoked by phenylhydrazine and bleeding provoked by repeated phlebotomies.Hepcidin response to hypoxia was also studied, both ex vivo, in human hepatoma cells, and in vivo.Anemia and hypoxia were associated with a dramatic decrease in liver hepcidin gene expression, which may account for the increase in iron release from reticuloendothelial cells and increase in iron absorption frequently observed in these situations.A single injection of turpentine for 16 hours induced a sixfold increase in liver hepcidin mRNA levels and a twofold decrease in serum iron.The hyposideremic effect of turpentine was completely blunted in hepcidin-deficient mice, revealing hepcidin participation in anemia of inflammatory states.These modifications of hepcidin gene expression further suggest a key role for hepcidin in iron homeostasis under various pathophysiological conditions, which may support the pharmaceutical use of hepcidin agonists and antagonists in various iron homeostasis disorders.
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In the citing paper
“the turpentine-induced hypoferremia was not observed in hepcidin-deficient mice (8), demonstrating that hepcidin is required for iron sequestration during inflammatory conditions”
From IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin (2004) · cites this paper as [8]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“hepcidin synthesis is regulated by dietary iron and iron stores, as well as by tissue oxygenation”
From IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin (2004) · cites this paper as [8]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“decreased in mice with anemia caused by bleeding or hemolysis or in mice with hypoxemia due to decreased ambient oxygen”
From IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin (2004) · cites this paper as [8]
The cited source says what the claim attributes to it.
In the citing paper
“injections of turpentine increased hepcidin mRNA”
From IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin (2004) · cites this paper as [8]
The cited source says what the claim attributes to it.
In the citing paper
“decreased serum iron”
From IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin (2004) · cites this paper as [8]
In the citing paper
“Infection and inflammation induce hepcidin production, driving a decrease in plasma iron concentrations by inhibiting the absorption of iron and promoting the sequestration of iron in macrophages.”
From Iron homeostasis in host defence and inflammation (2015) · cites this paper as [26]
In the citing paper
“The increase in hepcidin secretion in response to infectious or inflammatory stimuli is responsible for the characteristic hypoferraemia of inflammation26,27, which develops within a few hours of a systemic infection or following injection of microbial components or certain cytokines.”
From Iron homeostasis in host defence and inflammation (2015) · cites this paper as [26]
In the citing paper
“Strikingly, anaemia and anoxia both suppress hepcidin production [245,339,340] (Fig 3), such that just while superoxide production is being enhanced by the anoxia there is more iron being absorbed from the intestine and effluxed into the circulation.”
In the citing paper
“A common mechanism of hypoferremia of inflammation is a cytokine-driven increase in hepcidin [15] that downregulates ferroportin and thereby decreases iron flow into extracellular fluid from all its sources.”
From Iron and infection (2018) · cites this paper as [15]
In the citing paper
“Thus, under the influence of increased concentrations of hepcidin, recycled iron is retained in macrophages of the liver and the spleen, and iron absorption is decreased.”
From Iron and infection (2018) · cites this paper as [15]
In the citing paper
“Conversely, hepcidin expression is inhibited by hypoxia and erythropoiesis [11,12].”
From Hepcidin and Host Defense against Infectious Diseases (2015) · cites this paper as [11]
In the citing paper
“In addition, the amount of hepcidin mRNA in liver cells is decreased in response to hypoxia and ineffective erythropoiesis (overlapping with the response to iron deficiency) 99,105 and induced in response to treatment with lipopolysaccharide or by inflammation of other etiologies.92,99”
From Forging a field: the golden age of iron biology. (2008) · cites this paper as [99]
In the citing paper
“Initially, murine hepcidin mRNA was shown to be elevated in response to iron overload 92 and decreased in response to iron deficiency.99,100”
From Forging a field: the golden age of iron biology. (2008) · cites this paper as [99]
In the citing paper
“Experimental studies in cultured cells, in animal models and in human subjects have established that hepcidin production is O2-sensitive and involves the HIF pathway.”
From Regulation of erythropoiesis by hypoxia-inducible factors (2013) · cites this paper as [192]
In the citing paper
“A study that examined postmortem unfixed frozen brain sections from elderly normal or PD-affected individuals showed that individual neurons from brains of individuals with PD had significantly elevated iron concentrations (220).”
From Intracellular iron transport and storage: from molecular mechanisms to health implications (2008) · cites this paper as [220]
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Metadata
- Authors
- Nicolas, G., Chauvet, C., Viatte, L., Danan, J. L., Bigard, X., Devaux, I., Beaumont, C., Kahn, A., & Vaulont, S.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Service de Santé des Armées (FR)
- Inserm (FR)
- Corresponding author
- Vaulont, Sophie
- Venue
- Journal of Clinical Investigation
- Published
- 2002-10-01
- Volume
- 110
- Issue
- 7
- Pages
- 1037-1044
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W4243766541
- Cited by
- 1,214
- References
- 14
- Citations by year
- 2026: 11 · 2025: 23 · 2024: 16 · 2023: 36 · 2022: 33 · 2021: 35 · 2020: 63 · 2019: 52 · 2018: 53 · 2017: 55 · 2016: 44 · 2015: 45 · 2014: 71 · 2013: 58 · 2012: 61
- FWCI
- 20.80
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Funders
- Institut National de la Santé et de la Recherche Médicale
- Fondation pour la Recherche Médicale
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Ferroptosis and cancer prognosis
- Keywords
- hepcidin, iron homeostasis, anemia, hypoxia, inflammation, iron deficiency, iron overload, phlebotomy, turpentine, hepatoma cells, serum iron, reticuloendothelial cells
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