The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index; 11 of the 30 sources its claims cite were checked for support.
IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin
Open accessAbstract
Hypoferremia is a common response to systemic infections or generalized inflammatory disorders.In mouse models, the development of hypoferremia during inflammation requires hepcidin, an iron regulatory peptide hormone produced in the liver, but the inflammatory signals that regulate hepcidin are largely unknown.Our 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-hepcidin axis is responsible for the hypoferremia of inflammation. Methods Macrophage culture.Monocytes from peripheral blood were isolated by centrifugation through Ficoll-Paque (Amersham Pharmacia Biotech, Piscataway, New Jersey, USA) and 46% iso-Nonstandard abbreviations used: anemia of inflammation (AI); Iscove's modified Dulbecco's medium (IMDM); medium from LPS-stimulated macrophages (M-LPS); medium from unstimulated macrophages (M); recombinant human IL-6 (rhIL-6); total iron-binding capacity (TIBC); unsaturated iron-binding capacity (UIBC). Conflict of interest:The authors have declared that no conflict of interest exists.
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Claims the paper makes
23 Own result · 13 No full text of the sources · 13 Own interpretation · 6 Supported · 3 Partly supported · 1 Couldn’t confirm · 1 No basis given · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“patients with AI due to inflammatory disorders or infections had markedly increased excretion of urinary hepcidin”
What the sources say
- Supportedcites [12] source
The Results and discussion report elevated urinary hepcidin excretion in patients diagnosed with anemia of inflammation compared with healthy subjects and other patient groups. The same section reports very high excretion in a patient with epididymitis and sepsis, supporting the infection component of the claim. (LLM, conf=0.93)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“decreased serum iron”
What the sources say
- Supportedcites [8] Nicolas, 2002, J. Clin. Invest. source
The Results section reports a twofold decrease in serum iron in wild-type mice 16 hours after turpentine injection (Figure 6a). It also notes that this decrease was not observed in hepcidin-deficient mice. (LLM, conf=0.95)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“injections of turpentine increased hepcidin mRNA”
What the sources say
- Supportedcites [8] Nicolas, 2002, J. Clin. Invest. source
The Results section reports a sixfold increase in liver hepcidin gene expression 16 hours after turpentine injection compared with saline-injected controls. The discussion (p. 1042) explicitly describes this as a sixfold increase in liver hepcidin mRNA in mice. (LLM, conf=0.95)
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- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“strong induction of hepcidin mRNA by IL-6”
What the sources say
- Supportedcites [12] source
The Results and discussion section reports that IL-6 induced hepcidin in primary human hepatocytes within 8 hours, with a 25-fold increase. The Figure 2 caption identifies the measured signal as hepcidin mRNA. (LLM, conf=0.94)
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“but not IL-1 α or TNFα”
What the sources say
- Supportedcites [12] source
The Results and discussion section reports that IL-1α and TNF-α did not induce hepcidin mRNA within eight hours in primary human hepatocytes, unlike IL-6. It also notes that IL-1α induced hepcidin mRNA after 24 hours, probably indirectly through IL-6; the claim is consistent with the lack of strong direct induction. (LLM, conf=0.90)
plain- Asserted: passes — The authors put it forward as true.
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- Supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“LPS treatment increased hepcidin mRNA levels in primary human hepatocytes”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Anti-TNFα Ab's had no detectable effect in either experiment”
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Hep3B hepcidin mRNA, however, markedly increased after exposure to M-LPS”
plaindirectn = 4- Asserted: passes — The authors put it forward as true.
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In the paper
“Anti-IL-6 Ab's had similar inhibitory effects when hepatocytes or Hep3B cells were treated with conditioned medium from macrophages exposed to peptidoglycan from Staphylococcus aureus”
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“in IL-6 KO mice hepcidin mRNA increased ninefold”
plaindirect- Asserted: passes — The authors put it forward as true.
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- Probably not a substantial claim. 10
- It may state two separate claims as one. 17
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“hepcidin synthesis is regulated by dietary iron and iron stores, as well as by tissue oxygenation”
What the sources say
- Not checked — no full text of the sourcecites [3] source
- Partly supportedcites [7] sourceExperimental — accuracy not yet measured
Section 3.4 reports increased liver HEPC1 and HEPC2 transcripts in mice given dietary carbonyl iron or injected iron–dextran, supporting regulation by iron excess. The paper does not establish regulation by iron stores specifically, and no passage addresses tissue oxygenation; it measures gene expression rather than hepcidin synthesis directly. (LLM, conf=0.88)
- Partly supportedcites [8] Nicolas, 2002, J. Clin. Invest. sourceExperimental — accuracy not yet measured
The hypoxia results report that reduced tissue oxygenation downregulated hepcidin gene expression in mice. The anemia results show that iron loading increased expression, and the Discussion links iron deficiency to low expression until stores are repleted. The paper does not show that dietary iron itself regulates hepcidin synthesis; it describes hepcidin regulating dietary iron absorption instead. (LLM, conf=0.87)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“the turpentine-induced hypoferremia was not observed in hepcidin-deficient mice (8), demonstrating that hepcidin is required for iron sequestration during inflammatory conditions”
What the sources say
- Partly supportedcites [8] Nicolas, 2002, J. Clin. Invest. sourceExperimental — accuracy not yet measured
The results and discussion (p. 1042) report that turpentine lowered serum iron in wild-type mice but not in hepcidin-deficient mice. They establish hepcidin’s role in the inflammatory fall in serum iron, but describe iron sequestration as a proposed mechanism, not one directly demonstrated by that experiment. (LLM, conf=0.84)
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“hepcidin mRNA expression was increased in mice with dietinduced or genetically induced iron overload”
What the sources say
- Not checked — no full text of the sourcecites [3] source
- Partly supportedcites [7] sourceExperimental — accuracy not yet measured
Section 3.4 reports increased liver HEPC1 and HEPC2 transcripts in mice given dietary carbonyl iron, supporting the diet-induced part. The paper does not report increased hepcidin mRNA in genetically iron-overloaded mice; its Introduction instead describes iron overload in USF2 knockout mice that lack hepcidin transcripts. Page numbers are not available in our copy. (LLM, conf=0.87)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
Every source the paper cites for this claim was checked and supports it.
In the paper
“decreased in mice with anemia caused by bleeding or hemolysis or in mice with hypoxemia due to decreased ambient oxygen”
What the sources say
- Supportedcites [8] Nicolas, 2002, J. Clin. Invest. source
In “Hepcidin gene expression is decreased after experimentally induced anemia,” the paper reports reduced liver hepcidin mRNA after bleeding and reduced hepcidin expression after PHZ-induced hemolytic anemia. In “Hepcidin gene expression is tightly controlled by hypoxia,” it reports downregulation in mice exposed to reduced oxygen pressure in a hypobaric chamber. The hypoxic reduction was clear after two and four days, though results varied after twelve days. (LLM, conf=0.93)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“in the most common form of hemochromatosis, that caused by mutations in the HFE gene”
What the sources say
- Not checked — no full text of the sourcecites [11] source
- Could not verifycites [12] sourceExperimental — accuracy not yet measured
The Results and discussion (page unavailable) compare urinary hepcidin in patients with well-controlled hereditary hemochromatosis with levels in patients with anemia of inflammation, but do not say hepcidin production is diminished relative to healthy people. A search for HFE mutations found no passage identifying the hemochromatosis patients as having HFE-related disease. (LLM, conf=0.76)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“IL-6 infusion rapidly increased hepcidin excretion (Figure 4B); within 2 hours after the infusion, urinary hepcidin levels were 7.5-fold higher on average than at 0 hours”
plaindirectn = 6- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“serum iron decreased on average 34% and transferrin saturation decreased 33% in comparison to preinfusion values”
plaindirectn = 6- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“TNFα markedly suppressed hepcidin mRNA levels by a mechanism that did not involve IL-6 regulation”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“both the effects of LPS on primary human hepatocytes and the effects of M-LPS on Hep3B cells were completely reversed when IL-6-neutralizing Ab's were added”
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“median haptoglobin mRNA was 9.3-fold higher in turpentine-treated WT mice but only 1.9-fold higher in IL-6 KO mice”
plainn = 13- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The inflammatory and iron pathways of hepcidin stimulation respond rapidly, with major hepcidin increase detectable within 1 day in both humans and mice”
plaindirectn = 5 ·- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“hepcidin mRNA was increased in the livers of LPS-treated mice and in LPS-treated hepatocytes”
What the sources say
- Not checked — no full text of the sourcecites [3] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“There is a single human hepcidin gene whose essential role in iron homeostasis was confirmed by identifying homozygous frameshift or nonsense mutations in affected individuals with severe juvenile hemochromatosis”
What the sources say
- Not checked — no full text of the sourcecites [9] source
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“in transgenic mice overexpressing hepcidin-1 (4), transplacental and intestinal iron transport was blocked, and the mice died at birth from severe iron deficiency unless given parenteral iron supplementation”
What the sources say
- Not checked — no full text of the sourcecites [4] source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These observations suggest that human hepcidin is the functional equivalent of hepcidin-1 in mice.”
hedged- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Overexpression of the other known murine hepcidin gene, hepcidin-2, had no effect on iron metabolism in mice”
What the sources say
- Not checked — no full text of the sourcecites [6] source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Hepcidin production was also diminished in another form of juvenile hemochromatosis due to mutations in the hemojuvelin gene”
What the sources say
- Not checked — no full text of the sourcecites [10] source
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Hepatic hepcidin mRNA levels in mice were shown to increase in response to increased dietary iron”
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In IL-6 KO mice, however, hepcidin mRNA was suppressed, likely due to the negative regulation of hepcidin synthesis by other acute-phase cytokines”
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“changes in serum iron concentrations reflected the pattern of hepcidin induction: turpentine treatment caused serum iron decrease in WT mice, but no change in iron levels was detected in IL-6 KO mice”
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the decrease in iron supply becomes a bottleneck for hemoglobin synthesis and eventually results in anemia”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“When the rate of iron release from macrophages drops, plasma iron concentrations rapidly decrease”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“there are at least three major and distinct pathways of regulation of hepcidin: regulation by inflammation, dependent on IL-6; regulation by iron, dependent on some other factor, perhaps transferrin saturation; and suppression of hepcidin production during hypoxia and anemia”
hedgeddirectn = 5- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“transgenic overexpression of IL-6 in mice (36) and repeated administration of IL-6 in rats and cancer patients (33) has been reported to cause anemia”
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
IL-6 KO mice do not produce functional IL-6.
“Two pairs of IL-6 -/- (IL-6 KO) mice on a C57BL/6 background”
The paper relies on this without support.
Hepatic hepcidin mRNA levels reflect hepcidin synthesis or activity.
“Median hepcidin-1 expression in the liver increased 12-fold”
The paper relies on this without support.
Turpentine-induced inflammation in mice is a valid model of human inflammatory hypoferremia.
“we used the turpentine-induced mouse model of inflammation”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“increased concentrations of hepcidin then inhibit ferroportin activity”
From Hepcidin-Ferroportin Interaction Controls Systemic Iron Homeostasis (2021) · cites this paper as [52]
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
“leading to depletion of iron in plasma and extracellular fluid (hypoferremia).”
From Hepcidin-Ferroportin Interaction Controls Systemic Iron Homeostasis (2021) · cites this paper as [52]
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
“As a consequence of this interaction, the absorption of iron from the diet is reduced due to hepcidin mediated reduction of ferroportin expression in enterocytes, thereby resulting in a reduction of circulating iron levels which is further aggravated by the inhibition of iron export from macrophages by the same mechanism (Nemeth et al., 2004a; Kemna et al., 2005; Roy et al., 2007; Theurl et al., 2”
From Iron at the interface of immunity and infection (2014) · cites this paper as Nemeth et al., 2004a
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Infection and inflammation induce hepcidin, predominantly through the effects of the cytokine interleukin-6 (IL-6) [52]”
From Hepcidin-Ferroportin Interaction Controls Systemic Iron Homeostasis (2021) · cites this paper as [52]
The cited source says what the claim attributes to it.
In the citing paper
“Blockade of IL-6 receptor signaling prevented the hepatocyte-derived generation of hepcidin, which interferes with iron absorption (Nemeth et al., 2004”
From Targeting Interleukin-6 Signaling in Clinic (2019) · cites this paper as Nemeth et al., 2004
In the citing paper
“Interleukin-6 (IL-6) is the main cytokine that stimulates hepcidin synthesis during infection19 and inflammation, but other factors can also contribute, including activin B20, type I interferons (IFNs)21,22 and BMP2 (REF. 23).”
From Iron homeostasis in host defence and inflammation (2015) · cites this paper as [19]
In the citing paper
“Proinflammatory cytokines induced by inflammation can stimulate anemia of inflammation by limiting serum iron and increasing cellular iron stores by modulating the expression and activity of various iron regulatory proteins including hepcidin, FPN, ferritin, and the iron importer divalent metal transporter 1 (DMT1) [25–30].”
From The utility of iron chelators in the management of inflammatory disorders (2015) · cites this paper as [25]
In the citing paper
“However, hepcidin is overexpressed in inflammatory disease and is an early inflammatory marker [245,341-345].”
In the citing paper
“during an inflammatory episode interleukin-6 (IL-6) signals to the liver to release the hormone hepcidin, which promotes iron accumulation in phagocytic cells by inducing degradation of the iron exporter ferroportin (Fpn1) (Nemeth et al., 2004).”
From The Impact of Dietary Transition Metals on Host-Bacterial Interactions (2018) · cites this paper as Nemeth et al., 2004
In the citing paper
“The inflammatory increase in hepcidin is mainly caused by increased concentrations of IL-6 (interleukin-6) [19], inducing the transcription of the hepcidin gene through the JAK2/STAT3 [20][21][22] pathway.”
From Iron and infection (2018) · cites this paper as [19]
In the citing paper
“The role of IL-6 is important in many models of infection and inflammation [19,24] but in some models other cytokines may partially replace its stimulatory effect on hepcidin [17].”
From Iron and infection (2018) · cites this paper as [19]
In the citing paper
“One main contributing factor to pathologic iron homeostasis is interleukin (IL)-6 mediated induction of hepcidin expression through the Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) pathway [154].”
From Iron in immune cell function and host defense (2021) · cites this paper as [154]
In the citing paper
“During inflammation, HAMP is induced in hepatocytes alongside a battery of other acute‐phase proteins, downstream of interleukin‐6 and toll‐like receptor signalling‐associated pathways. 98”
From The battle for iron in enteric infections (2020) · cites this paper as [98]
In the citing paper
“To correct this, all animals were conditioned on a low-iron diet (2-4 ppm iron; Teklad diet TD.80396, Envigo) for 5-7 days prior to, and throughout the duration of, all experiments.”
From Hepcidin-mediated iron sequestration protects against bacterial dissemination during pneumonia (2017) · cites this paper as [43]
In the citing paper
“Accordingly, IL6 is a key mediator of inflammation-driven iron handling, as it induces the production of hepcidin, the master regulator of iron homeostasis [4].”
In the citing paper
“It has been suggested that the COVID-19 related inflammation may be the main cause of COVID-19 associated iron disorders, as an inflammation-driven dysregulation of iron homeostasis is well established [4, 6, 7].”
In the citing paper
“The study of hepcidin regulation in mice housed under standard conditions is confounded by the high iron content of most commercial mouse chow blends.”
From Hepcidin and Host Defense against Infectious Diseases (2015) · cites this paper as [16]
In the citing paper
“Sustained elevation of hepcidin expression, as occurs in many inflammatory states, results in anemia due to reduced availability of iron for erythropoiesis, a condition previously known as “anemia of chronic disease” and more accurately renamed as “anemia of inflammation” [16,22,23].”
From Hepcidin and Host Defense against Infectious Diseases (2015) · cites this paper as [16]
In the citing paper
“In animal models, diverse inflammatory and infectious stimuli, including Streptococcus species, Pseudomonas aeruginosa, Aspergillus fumigatus, influenza, turpentine, and lipopolysaccharide (LPS) robustly induce hepcidin in the liver via the induction of IL-6, resulting in rapid reduction in serum iron levels [16,19–21].”
From Hepcidin and Host Defense against Infectious Diseases (2015) · cites this paper as [16]
In the citing paper
“In the context of inflammation, IL-6 and IL-22 stimulate HAMP expression via specific receptors signaling through signal transducer and activator of transcription (STAT)-3, while alpha-1 antitrypsin may do so via HJV and matriptase-2 [69–71].”
From Iron deficiency or anemia of inflammation?: Differential diagnosis and mechanisms of anemia of inflammation (2016) · cites this paper as [70]
In the citing paper
“but is also an acute phase protein upregulated by inflammatory cytokines, notably IL-6 [18–20].”
From Rapidly Escalating Hepcidin and Associated Serum Iron Starvation Are Features of the Acute Response to Typhoid Infection in Humans (2015) · cites this paper as [19]
In the citing paper
“During neuroinflammation, glial cells are activated, which perturbs iron homoeostasis.34,35”
From The role of iron in brain ageing and neurodegenerative disorders (2014) · cites this paper as [35]
In the citing paper
“Serum sTR concentration reflects total erythroid activity and iron status and has been shown to reflect plasma iron turnover and erythroid transferrin uptake if iron deficiency is not present (22,25).”
From Testosterone induces erythrocytosis via increased erythropoietin and suppressed hepcidin: evidence for a new erythropoietin/hemoglobin set point (2014) · cites this paper as [22]
In the citing paper
“Serum sTR concentration reflects total erythroid activity in rats and humans and has been shown to reflect plasma iron turnover and erythroid transferrin uptake very closely if iron deficiency is not present (22).”
From Testosterone induces erythrocytosis via increased erythropoietin and suppressed hepcidin: evidence for a new erythropoietin/hemoglobin set point (2014) · cites this paper as [22]
In the citing paper
“We found that the hepatocytelike cells of the adenomas expressed very high levels of hepcidin 100 and speculated that our results could be generalized-that induction of hepcidin expression in response to inflammation might explain the anemia of chronic disease.”
From Forging a field: the golden age of iron biology. (2008) · cites this paper as [197]
In the citing paper
“In mice, HFE2 is localized to the surface of periportal hepatocytes, and HFE2-mutant mice display iron loading and a striking decrease in hepcidin upregulation in response to increased iron from exogenous sources, compared with controls (217).”
From Intracellular iron transport and storage: from molecular mechanisms to health implications (2008) · cites this paper as [217]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
“Six healthy volunteers collected first morning urine for 9 days.”
“Five subjects took 65 mg of iron (as ferrous sulfate) for 3 days, and their urinary hepcidin was monitored before, during, and after iron supplementation.”
Citations
Cites
A new mathematical model for relative quantification in real-time RT-PCR
Pfaffl, M. W. (2001) · Nucleic Acids Research · doi:10.1093/nar/29.9.e45 · Cited by 34,610
Targeting Hypoxia-Inducible Factors for the Treatment of Anemia in Chronic Kidney Disease Patients
Locatelli, F., Fishbane, S. N., Block, G. A., & Macdougall, I. C. (2017) · American Journal of Nephrology · doi:10.1159/000455166 · Cited by 4,836
Weiss, G., & Goodnough, L. T. (2005) · New England Journal of Medicine · doi:10.1056/nejmra041809 · Cited by 3,800
Hepcidin, a urinary antimicrobial peptide synthesized in the liver
Park, C. H., Valore, E. V., Waring, A. J., & Ganz, T. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m008922200 · Cited by 2,168
Self-citationAndrews, N. C. (1999) · New England Journal of Medicine · doi:10.1056/nejm199912233412607 · Cited by 2,130
Pigeon, C., Ilyin, G., Courselaud, B., Leroyer, P., Turlin, B., Brissot, P., & Loréal, O. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m008923200 · Cited by 1,697
Hepcidin, a key regulator of iron metabolism and mediator of anemia of inflammation
Ganz, T. (2003) · Blood · doi:10.1182/blood-2003-03-0672 · Cited by 1,544
Self-citationHepcidin, 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
Krause, A., Neitz, S., Mägert, H.-J., Schulz, A., Forssmann, W.-G., Schulz-Knappe, P., & Adermann, K. (2000) · FEBS Letters · doi:10.1016/s0014-5793(00)01920-7 · Cited by 1,324
Age-Associated Increased Interleukin-6 Gene Expression, Late-Life Diseases, and Frailty
Ershler, W. B., & Keller, E. T. (2000) · Annual Review of Medicine · doi:10.1146/annurev.med.51.1.245 · Cited by 1,282
Research works printed but not linked: 2
- Means, 1999, Int. J. Hematol., 70, 7
- Barille, 2000, Eur. Cytokine Netw., 11, 546
Cited by
Sorted by citations
Items 2,501–2,600 of 2,683
The Dysregulation of Iron Homeostasis in Obesity
Ramasamy, J. (2025) · Springer eBooks · doi:10.1007/978-3-031-32047-7_115-1 · Cited by 1
Choi, S., Kim, K., Kwak, J., Lee, J. Y., Taeho, L. E. E., Kim, M., Yun, Y., & Song, W. (2026) · Journal of Veterinary Clinics · doi:10.17555/jvc.2026.43.2.79
Li, X., Shi, Q., Wang, Z., Zhang, Z., & Li, M. (2026) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2026.1761986
“This favors intracellular iron retention and links inflammation to cellular iron loading and oxidative lipid damage (71 – 73).”
Para, N. K. O., Koshy, G., & Rab, S. (2026) · Cureus · doi:10.7759/cureus.109279
“At the molecular level, interleukin-6 (IL-6) activates the JAK-STAT3 signaling pathway, leading to transcriptional upregulation of ferritin heavy chain genes, while tumor necrosis factor-alpha (TNF-α ) activates NF-κ B signaling, further enhancing ferritin synthesis [4,5].”
Potential Usefulness of Urinary Hepcidin Measurement for Iron Deficiency Anemia in Female Athletes
Hanawa, H., Inaba, H., Hoshino, F., Edama, M., Sekine, C., Kikumoto, T., Ishigaki, T., Matsuura, Y., & Omori, G. (2026) · European Journal of Sport Science · doi:10.1002/ejsc.70198
“On the other hand, inflammation is known to increase inflammatory cytokines such as IL‐6, which enhance hepcidin expression (Nemeth, Rivera, et al. 2004).”
Imani, A., Prajoko, Y. W., Nirwantono, R., Mozar, F. S., Pardamean, B., & Limijadi, E. K. S. (2026) · Oncology Reviews · doi:10.3389/or.2026.1818926
“Inflammatory cytokines could interfere with iron metabolism and erythrocyte maturation, leading to subtle reductions in erythrocyte size (47).”
Anaplasma phagocytophilum subversion of host hepcidin-ferroportin iron nutritional immunity
Denton, S. L., Lin, M., Nemeth, E., & Rikihisa, Y. (2026) · mBio · doi:10.1128/mbio.01134-26
“In vitro stimulation of fresh human hepatocytes with a panel of cytokines showed strong induction of Hepc mRNA by IL-6, but not IL-1α or TNF-α (75), indicating that IL-6 is a primary proinflammatory mediator of Hepc induction at a local level (60).”
Self-citationLucernoni, K. M., Chacon, S. J., Needham, K. W., Halliwill, J. R., & Minson, C. T. (2026) · Physiological Reports · doi:10.14814/phy2.70981
“Interluekin-6 (IL-6) has been identified as an important inflammatory and energy sensing cytokine that regulates production of hepcidin (Lee et al., 2005; Nemeth et al., 2004; Nemeth & Ganz, 2009).”
Mitsuura, C., Ida, S., Tsubakihara, H., Yamashita, K., Eto, K., Matsumoto, C., Kosumi, K., Harada, K., Miyamoto, Y., & Iwatsuki, M. (2026) · Gastric Cancer · doi:10.1007/s10120-026-01783-2
Webb, B., Farrell, M., Montelius, C., & Önning, G. (2026) · Frontiers in Nutrition · doi:10.3389/fnut.2026.1905459
Aguree, S., Turi, K. N., Handt, A., Kohut, M., & Reddy, M. B. (2026) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.70575
Rahat, M. R. H., Haque, M. I., Shurmi, S. D., Hossain, A., Fahim, M., Muhammad, A. B., Bahar, N. I., Islam, M. E., Islam, R., Kamruzzaman, M., et al. (2026) · Anemia · doi:10.1155/anem/8514650
“Beyond cardiovascular risk, trans fat-rich diets are characteristically proinfammatory [26], and chronic low-grade infammation has been recognized as a suppressor of erythropoiesis through mechanisms, including hepcidin upregulation [27], which restricts iron availability for Hb synthesis.”
Cyclical Iron Homeostasis: The Role of Sex Hormones in Female Iron Regulation
Balakirishnan, D., Dukovski, F., Bytheway, H. G., & Dugan, C. (2026) · Frontiers in Bioscience-Landmark · doi:10.31083/fbl54404
Maimaiti, Y., Guo, Z., Tian, Y., Lu, P., Nannan, W., Wang, S., Xu, H., Chu, H., & Wang, Y. (2026) · Research Square · doi:10.21203/rs.3.rs-11025140/v1
Jain, D., Gupta, A., Agarwal, V., Singh, B. K., Chaudhary, A., & Kumar, P. (2026) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-026-05964-9
La homeostasis del hierro y una hormona: la hepcidina.
Barrios, Y., Acosta, E., Espinoza, M., Meléndez, A., & Méndez, D. (2007) · Redalyc (Universidad Autónoma del Estado de México)
Poziom surowiczego białka C-reaktywnego (CRP) i wskaźników hematologicznych u prosiąt
Warmińsko-Mazurski, U., Genetyki, K., & Oczapowskiego, M. (2012) · Roczniki Naukowe Polskiego Towarzystwa Zootechnicznego
О возможности влияния микроорганизмов на гомеостаз железа в организме хозяина (обзор литературы)
Leonov, V. V., Курлович, Н. А., Леонова, Л. В., & Фатеева, Н. М. (2014) · DOAJ (DOAJ: Directory of Open Access Journals)
Micronutrients, Trace Elements
Cousins, R. J. (2006) · Wiley-VCH eBooks · doi:10.1002/3527600906.mcb.200400037
Iron Homeostasis: Hepcidin Regulation
Camaschella, C., & Silvestri, L. (2004) · Wiley eBooks · doi:10.1002/9781119951438.eibc2131
Development of Anticytokine Agents for Rheumatoid Arthritis
Sherlock, J., Buckley, C., & Raza, K. (2011) · Wiley eBooks · doi:10.1002/9780470571224.pse455
Extraintestinal Consequences of Mucosal Inflammation
Bourikas, L. A., & Papadakis, K. A. (2010) · Wiley eBooks · doi:10.1002/9781444318418.ch14
Avaliação da expressão de hepcidina e produção de IL-6 por monócitos de indivíduos idosos
Miranda, J. C. (2009) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/d.60.2009.tde-25082009-152450
Status de ferro em pacientes com insuficiência cardíaca avançada
da Silva, J. H. (2013) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/d.89.2013.tde-28052015-113838
Ilkovska, B., Trifunova, B. K., & Трифунов, Г. (2015) · Macedonian Medical Electronic Journal · doi:10.3889/mmej.2015.50010
Iron Overload in Patients Receiving Allogeneic Hematopoietic Stem Cell Transplantation
Busca, A., Dellacasa, C. M., & Pecoraro, C. (2014) · Global Journal of Hematology and Blood Transfusion · doi:10.15379/2408-9877.2014.01.02.03
Crichton, R. R. (2016) · Wiley eBooks · doi:10.1002/9781118925645.ch12
Evaluation of serum hepcidin in assessment of iron status in renal transplant patients
El-Khatib, M. M., Fawzy, M., Khashab, S., Ramzy, M. F., Elgayar, D. F., & Kamal, M. (2010) · African Journal of Nephrology · doi:10.21804/14-1-770
Salam, R., Gamil, G. E., Sabry, D., Nassar, Y., Ibrahem, M., Hassan, E., Araf, W., Mazny, A. E., & Ahmed, S. (2016) · Kasr Al Ainy Medical Journal · doi:10.4103/1687-4625.188605
Porbén, S. I. S., Fernández, E. P., García, R. J., Fallas, S. M. R., & Fallas, R. (2016) · DOAJ (DOAJ: Directory of Open Access Journals) · doi:10.19230/jonnpr.2016.1.6.1081
Potential Role of Chloroquine in Macrophageal Iron Mobilization
Nweneka, C. V. (2016) · Pharmaceutica Analytica Acta · doi:10.4172/2153-2435.1000505
АНЕМИЯ У ВИЧ-ИНФИЦИРОВАННЫХ ПАЦИЕНТОВ. ПАТОГЕНЕЗ И СОВРЕМЕННАЯ ТЕРАПЕВТИЧЕСКАЯ ТАКТИКА
Александровна, Г. Л., Иванович, М. В., Борисович, М. В., & Russian Federation (2014) · Вестник Санкт-Петербургского университета. Серия 11. Медицина
Teles, A. V. F. F. (2017) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/t.10.2017.tde-25042017-110126
Inoyаtova, F. I., Kadyrkhodjaeva, K. M., Иногамова, Г. З., Akhmedovа, A. K., Валиева, Н. К., Abdullaevа, F. G., & Anvarovna, I. N. (2017) · CHILDREN INFECTIONS · doi:10.22627/2072-8107-2017-16-3-24-27
Bassi, G. S. (2017) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/t.17.2017.tde-06012017-165821
Hematological Manifestations of Infectious Disease
Sanjeevaiah, A. R. (2018) · JOJ Nursing & Health Care · doi:10.19080/jojnhc.2018.08.555727
A Case of Secondary Hemochromatosis with Elevated Serum Interleukin-6
TSUTSUMI, M., Nakamura, M., Kawazu, S., Ito, T., & Furue, M. (2019) · The Nishinihon Journal of Dermatology · doi:10.2336/nishinihonhifu.81.106
The Pediatric Patient with Chronic Kidney Disease
Warady, B. A., & Chadha, V. (2010) · Elsevier eBooks · doi:10.1016/b978-1-4377-0987-2.00017-0
Artuković, I., Mrljak, V., Lipar, M., Pavlak, M., Bedrica, L., & Rafaj, R. B. (2020) · Veterinarska stanica · doi:10.46419/vs.51.2.9
Are Hemochromatosis Mutations Protective Against Iron-Mediated Atherogenesis?
Jerome, L. (2012) · InTech eBooks · doi:10.5772/26199
Tarocchi, M. (2019) · Gastroenterology & Hepatology International Journal · doi:10.23880/ghij-16000161
Isibor, C. N., Okojie, R., Ophori, E. A., & Omonigho, S. E. (2020) · Libyan Journal of Medical Sciences · doi:10.4103/ljms.ljms_41_19
Абдуллаев, Р. Ю., Комиссарова, О. Г., & Терентьева, О. Р. (2021) · Вестник ЦНИИТ · doi:10.7868/s2587667821010015
The clinical and paraclinical efficacy of tocilizumab in juvenile idiopathic arthritis
Revenco, N., CRACEA, A., Mazur-Nicorici, L., Silvia, F. O. C. A., Eremciuc, R., GAIDARJI, O., IACOMI, V., & BOGONOVSCHI, L. (2021) · Archives of the Balkan Medical Union · doi:10.31688/abmu.2021.56.2.07
IRON HOMEOSTASIS REGULATING FACTORS IN HEPATITIS C
(2020) · Egyptian Journal of Applied Science · doi:10.21608/ejas.2020.136030
Research Progress of Renal Anemia and Iron Metabolism
刘, 静. (2022) · Advances in Clinical Medicine · doi:10.12677/acm.2022.121071
Nelson, J. E., Trinder, D., & Kowdley, K. V. (2010) · Molecular pathology library · doi:10.1007/978-1-4419-7107-4_44
Lackner, C., & Knisely, A. S. (2020) · Pathologie · doi:10.1007/978-3-642-04557-8_4
Napolitano, L. M. (2008) · Springer eBooks · doi:10.1007/978-0-387-68113-9_9
Sanford, A. M. (2022) · Wiley eBooks · doi:10.1002/9781119484288.ch22
Kamat, A. S., & Thomas, D. R. (2012) · Wiley eBooks · doi:10.1002/9781119952930.ch28
Red Blood Cell/Hemoglobin Disorders
Kroft, S. H., & Monaghan, S. A. (2012) · Elsevier eBooks · doi:10.1016/b978-1-4377-2606-0.00001-9
Iron Uptake in Host Defense Against Pneumonia
Michels, K. R. (2017) · doi:10.18130/v3465h
Immune System and Neuroinflammation
Crichton, R. R., & Ward, R. J. (2013) · Wiley eBooks · doi:10.1002/9781118553480.ch03
Saraf, S. L., & Gordeuk, V. R. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-805378-2.00006-1 · Cited by 1
Brandt, S., Takala, J. A., & Lepper, P. (2008) · Yearbook of intensive care and emergency medicine · doi:10.1007/978-3-540-77290-3_44
Iron Deficiency in Critically III Patients: Highlighting the Role of Hepcidin
Heming, N., Montravers, P., & Lasocki, S. (2011) · Annual update in intensive care and emergency medicine · doi:10.1007/978-3-642-18081-1_7
Ettle, T., Elsenhans, B., & Schümann, K. (2012) · Wiley eBooks · doi:10.1002/9783527653058.ch7
Importance of detection of hepsidine and interleukins in Iron deficiency anemia
Saydullaevich, M. L., Khaydarovna, M. F., Fakhruddinovna, K. D., & Ziyadullaevich, M. Z. (2022) · Asian Journal of Multidimensional Research · doi:10.5958/2278-4853.2022.00058.1
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Kalenderer, Ö., & Erkuş, S. (2022) · Biomarkers in disease · doi:10.1007/978-3-030-87302-8_32-1
Санталова, Г. В., & Валентиновна, П. С. (2022) · Meditsinskiy sovet = Medical Council · doi:10.21518/2079-701x-2022-16-12-173-177
Sakhin, V. T., Григорьев, М. А., Крюков, Е. В., Казаков, С. П., & Анатольевич, Р. О. (2020) · Гематология Трансфузиология Восточная Европа · doi:10.34883/pi.2020.6.1.014
Alfaro-Magallanes, V. M. (2022) · UPM Digital Archive (Technical University of Madrid) · doi:10.20868/upm.thesis.71841
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Mukhopadhyay, C. K., Mishra, P., Aggarwal, A., & Yadav, S. (2022) · Elsevier eBooks · doi:10.1016/b978-0-323-91305-8.00016-8
de França, F. S. (2021) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/t.42.2021.tde-04052022-155627
Kumar, M., Kundu, B. K., & Goyal, P. (2022) · Indian Journal Of Applied Research · doi:10.36106/ijar/2305847
Singh, J. K., Kumari, N., & Prasad, K. (2023) · International Journal of Pharmaceutical Sciences Review and Research · doi:10.47583/ijpsrr.2023.v79i01.021
Ma, C., Guo, X., Zhu, F., Ren, Y., Wang, H., Wang, M., & Qin, R. (2017) · Oncology and Translational Medicine · doi:10.1007/s10330-016-0232-2
Alsamarai, A. M., Hassan, H., & Alobaidi, A. H. (2019) · Aalborg Academy Journal of Medical Sciences · doi:10.32441/ijms.2.1.5
Zhang, W., Sun, J., Li, J., Wang, Y., Liu, W., Xue, W., Yuan, Y., & Wang, X. (2023) · Academic Radiology · doi:10.1016/j.acra.2023.09.006
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Sánchez‐Ramón, S., & Guzmán, M. G. (2023) · Springer eBooks · doi:10.1007/978-3-031-35225-6_17
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Gadaev, A. G., & Khujakulova, F. I. (2023) · Oriental Journal of Medicine and Pharmacology · doi:10.37547/supsci-ojmp-03-04-09
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Markousis-Mavrogenis, G. (2024) · doi:10.33612/diss.1035139595
Burrone, M., Martini, A., & Malattia, C. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-23947-2.00006-0
Singh, V. P., Pillai, A. N., Rajalingamgari, P., & Khatua, B. (2024) · Springer eBooks · doi:10.1007/978-981-97-3132-9_6
闫, 晓. (2024) · Advances in Clinical Medicine · doi:10.12677/acm.2024.1482230
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Yin, J. L., Raja, K. B., & Ala, A. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-26711-6.00029-9
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Aijima, R., Yamashita, R., Kamohara, A., Danjo, A., & Yamashita, Y. (2024) · Journal of Japanese Society of Oral Medicine · doi:10.6014/jjsom.30.25
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Gan, L., & Zuo, L. (2025) · Springer eBooks · doi:10.1007/978-981-97-7636-8_12
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Sedláčková, T., & Racek, J. (2009) · Klinická biochemie a metabolismus · doi:10.61568/kbm.2009.003
Spiro, S., Griffiths, A., Arnaout, A. H., Wrigglesworth, E., Macgregor, S. K., John, S. K., Tahas, S. A., Nye, E. L., & Morrell, A. P. (2025) · Veterinary Pathology · doi:10.1177/03009858251343017
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Effect of 2‐h hypoxic exposure on resting hepcidin levels in young adults
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Fujikawa, R., Nagano, N., Mitobe, Y., & Ito, K. (2025) · Clinical and Experimental Nephrology · doi:10.1007/s10157-025-02783-9
Metadata
- Authors
- Nemeth, E., Rivera, S., Gabayan, V., Keller, C., Taudorf, S., Pedersen, B. K., & Ganz, T.
- Affiliations
- University of California, Los Angeles (US)
- Rigshospitalet (DK)
- Corresponding author
- Ganz, Tomas
- Venue
- Journal of Clinical Investigation
- Published
- 2004-05-01
- Volume
- 113
- Issue
- 9
- Pages
- 1271-1276
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC398432
- OpenAlex
- W2132155262
- Cited by
- 2,650
- References
- 40
- Citations by year
- 2026: 100 · 2025: 97 · 2024: 93 · 2023: 117 · 2022: 115 · 2021: 145 · 2020: 134 · 2019: 130 · 2018: 130 · 2017: 141 · 2016: 103 · 2015: 135 · 2014: 132 · 2013: 140 · 2012: 137
- FWCI
- 55.20
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- David Geffen School of Medicine, University of California, Los Angeles
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Ferroptosis and cancer prognosis
- Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
- Keywords
- interleukin-6, hepcidin, iron regulation, inflammation, cytokine signaling, liver, iron regulatory hormone
- MeSH terms
- Anemia, Animals, Cell Line, Cells, Cultured, Gene Expression Regulation, Humans, Inflammation, Iron, Kupffer Cells, Mice, Inbred C57BL, Monocytes, RNA, Messenger, Interleukin-6, Mice, Knockout, Iron Metabolism Disorders, Reverse Transcriptase Polymerase Chain Reaction, Hepatocytes, Antimicrobial Cationic Peptides, Mice, Hepcidins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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