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
11 of 30 cited sources checked · 6 supported · 0 flagged · 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)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- 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)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- 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)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- 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)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- 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)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- 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”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA 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
“Anti-TNFα Ab's had no detectable effect in either experiment”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA 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”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA 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
“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”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA 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
“in IL-6 KO mice hepcidin mRNA increased ninefold”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes
- 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)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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”
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt 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”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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”
Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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.”
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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”
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt 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”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably 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”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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.
Human iron-supplementation participant count differs
MinorThe Methods section says six volunteers participated in the iron-supplementation study, while the Results section says five subjects took the iron supplements.
“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
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Hepcidin, a urinary antimicrobial peptide synthesized in the liver
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Hepcidin, a key regulator of iron metabolism and mediator of anemia of inflammation
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Self-citationHepcidin, a putative mediator of anemia of inflammation, is a type II acute-phase protein
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Self-citationLEAP-1, a novel highly disulfide-bonded human peptide, exhibits antimicrobial activity
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Age-Associated Increased Interleukin-6 Gene Expression, Late-Life Diseases, and Frailty
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Flagged first, then by citations
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“[32] Even if hepcidin expression is up-regulated by IL-6, CKD clinical studies are not consistent in supporting the correlation between hepcidin and IL-6.”
BackgroundImaeda, T., Nakada, T., Abe, R., & Oda, S. (2019) · PLoS ONE · doi:10.1371/journal.pone.0210067 · Cited by 3
Rheumatoid arthritis and myelodysplastic syndrome: a fortuitous association?
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BackgroundInfluentialAssociation between Serum Ferritin and Body Composition in Young Women
Dandekar, U. S. (2023) · ScholarWorks@UMassAmherst (University of Massachusetts Amherst) · doi:10.7275/981063 · Cited by 3
Iron Physiology and Its Impact on Atopic Diseases: An EAACI Taskforce Report
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Iron as an immunometabolic signal in infection and inflammation
Hoffmann, A., Pérez, L. H., & Weiss, G. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1810718 · Cited by 3
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THE EFFECT OF CHRONIC IRON LOSSES ON LIVER REGENERATION IN MALE AND FEMALE RATS
Živná, H., Živný, P., Vokurková, D., Švejkovská, K., & Palička, V. (2010) · Biomedical Papers · doi:10.5507/bp.2010.023 · Cited by 3
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Determinants of Anemia in Schoolchildren in the Highland Bolivia
Cuna, W. R., Contreras, I., Rodríguez, A., Passera, R., & Rodríguez, C. (2024) · Microorganisms · doi:10.3390/microorganisms12122491 · Cited by 3
“Ferroportin internalization and degradation are mediated by the regulatory protein hepcidin which is up-regulated by interleukin (IL) 6 during inflammation [29,30].”
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Lactobacillus acidophilus: Boosting Immunity Through IL-6 Induction
Adejumo, I. O. (2025) · Biologics · doi:10.3390/biologics5040029 · Cited by 3
The role of IL-6 in rheumatoid arthritis comorbidity and implications for therapy
Monaco, F., Dimonte, S., & Jones, S. A. (2026) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2026.120136 · Cited by 3
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The Utility of Immuno-Nutritional Scores in Patients with Testicular Germ Cell Tumors
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Intravenous iron treatment fuels chronic kidney disease‐induced arterial media calcification in rats
den Branden, A. V., Opdebeeck, B., Adriaensen, S., Evenepoel, P., Berghe, T. V., & Verhulst, A. (2024) · The Journal of Pathology · doi:10.1002/path.6375 · Cited by 3
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Iron Biology: Metabolism and Homeostasis
Ganz, T. (2022) · Nutrition and health · doi:10.1007/978-3-031-14521-6_2 · Cited by 3
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Anemia of inflammation: clinical insights from mechanisms.
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Urinary hepcidin concentration in assessment of iron homeostasis in pediatrics
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ДОНАЦІЇ КРОВІ І МЕТАБОЛІЗМ ЗАЛІЗА
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Iron Sequestration in Immunity
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Association between genetic variations in TFR2 gene and coronary heart disease in Chinese
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Differential diagnosis of anemia in pregnant women
Prokhorenko, T. S., Zima, A. P., Саприна, Т. В., Мусина, Н. Н., Shakhmanova, N. S., & Novitsky, V. V. (2017) · Bulletin of Siberian Medicine · doi:10.20538/1682-0363-2017-1-140-151 · Cited by 2
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“IL-6 contributes to the development of ACD by engaging in iron metabolism processes [23].”
Elbaset, M. A., El-Latif, N. A. A., Ibrahim, F. A., El‐Seidy, A. M. A., Moussa, S. A. A., & Bashandy, S. A. E. (2024) · Brazilian Archives of Biology and Technology · doi:10.1590/1678-4324-2024230333 · Cited by 2
“It has been established that IL-6 is both a required and sufficient cytokine for the induction of hepcidin during inflammation and that the IL-6-hepcidin axis is responsible for the hypoferremia seen in inflammatory diseases [59].”
Alharbi, M., Bawek, S. J., Lund, I., Glenn, S. T., Green, S. D., Hassan, H., Qian, Y., & Hillengass, J. (2025) · Annals of Hematology · doi:10.1007/s00277-025-06218-z · Cited by 2
“Another proposed theory is impairment of iron utilization due to the hepcidin upreg - ulation in patients with MM, which occurs as a result of elevated interleukin-6 (IL-6) levels [29 , 30 ].”
van Rensburg, S. J., van Toorn, R., Jaftha, M., Kemp, M. C., Engel-Hills, P. C., & Kotze, M. J. (2025) · Metabolic Brain Disease · doi:10.1007/s11011-025-01678-8 · Cited by 2
“IL-6 mediates hypoferremia of inflammation by inducing the synthesis of hepcidin (Nemeth et al. 2004 ).”
Anemia and Quality of Life: Association with Diagnosis and Treatment of Anemias
Thomas, D. R. (2009) · Springer eBooks · doi:10.1007/978-0-387-78665-0_111 · Cited by 2
The Effects of Treatment on Serum Hepcidin and Iron Homeostasis in HIV-1-Infected In-dividuals
da Cunha, J., Maselli, L. M. F., Ferreira, J. D. S., Spada, C., & Bydlowski, S. P. (2015) · World Journal of AIDS · doi:10.4236/wja.2015.53018 · Cited by 2
“Ferroportin is the only known cellular iron exporter, and it is essential for iron homeostasis [5].”
BackgroundRole of iron metabolism-regulator hepcidin in perinatal iron homeostasis
Balogh, Á., Bősze, S. E., Horváti, K., Mező, G., Kéki, S., Nagy, L., Bokodi, G., Szabó, M., & Vásárhelyi, B. (2010) · Orvosi Hetilap · doi:10.1556/oh.2010.28773 · Cited by 2
“Napjainkban csak egy-egy antitest alapú módszer létezik a vizelet, illetve a szérum hepcidin-szint mennyiségi meghatározására: a vizelet hepcidin meghatározására egy szemikvantitatív dot blot [48, 64] és a szérum hepcidin kimutatásra egy Western blot módszer [65].”
InfluentialSłomka, A., Koba, M., Kulwas, A., & Żekanowska, E. (2011) · Current Pharmaceutical Analysis · doi:10.2174/157341211796353309 · Cited by 2
“Finally, the inflammatory cytokine IL-6 (interleukin-6) may increased hepcidin through induction and subsequent promoter binding of signal transducer and activator of transcription 3 (STAT3) [41-43].”
BackgroundRole of hepcidin in the development of anemia in patients with rheumatoid arthritis
Galushko, E. A., Belenky, D. A., Александрова, Е. Н., & Kashnikova, L. N. (2012) · Rheumatology Science and Practice · doi:10.14412/1995-4484-2012-704 · Cited by 2
Is Hepcidin a Good Marker for Inflammation in Obstructive Sleep Apnea Syndrome (OSAS) Patients?
Fırat, H., Özdemir, C., Bilgin, E., Luyster, F. S., Yüceege, M., Kızılgün, M., Demır, A. U., Strollo, P. J., & Ardıç, S. (2015) · Journal of Turkish Sleep Medicine · doi:10.4274/jtsm.02.009 · Cited by 2
Aplastic and Hypoplastic Anemias
Noronha, S. A. (2018) · Pediatrics in Review · doi:10.1542/pir.2017-0250 · Cited by 2
Intravenous iron in patients with iron deficiency and heart failure: a review of modern evidence
Gale, S. E., Willeford, A., Sandquist, K., & Watson, K. (2024) · Current Opinion in Cardiology · doi:10.1097/hco.0000000000001121 · Cited by 2
Study on HIF-PHI combined with iron supplement in treatment of renal anemia in rats
Gao, Z., Gao, Y., Wang, Q., Wang, Q. M., Lu, P., Lv, H., Xue, H., Ma, X., Li, S., & Hu, Z. (2025) · BMC Nephrology · doi:10.1186/s12882-025-04045-y · Cited by 2
“Some studies have shown that hepcidin expression is regulated by inflammation and iron load [36, 37].”
Haematological parameters in erythropoietic protoporphyria: A multi‐national study
Leaf, R. K., Ricci, A., Tran, B., Corradini, E., Pietrangelo, A., Mancini, C., Garuti, C., Saltini, D., Schepis, F., Kubisch, I., et al. (2025) · British Journal of Haematology · doi:10.1111/bjh.20197 · Cited by 2
“19 Therefore, the laboratory values we observed seem more consistent with iron deficiency anaemia than anaemia of inflammation.”
Douba, Z. A., & Ibrahim, R. (2025) · Health Science Reports · doi:10.1002/hsr2.71148 · Cited by 2
“Hepcidin, regulates iron homeostasis by inhibiting iron absorption from the intestine and iron release from macrophages [77].”
InfluentialGaneb, S. S., Hammad, G. A., Eltanawy, R. M., Hashaad, N. I., Ahmed, I. A. E., Gomah, D. K., & Amer, A. S. (2016) · Egyptian Rheumatology and Rehabilitation · doi:10.4103/1110-161x.189827 · Cited by 2
Evaluation of serum hepcidin as a biochemical marker in diagnosis of anemia of chronic disease
Vyas, S., Suman, S., Kapoor, A., & Nema, S. (2018) · International Journal of Research in Medical Sciences · doi:10.18203/2320-6012.ijrms20182042 · Cited by 2
“The correlation coefficient was 0.6359 with significance level P 0.0001 at 95% confidence interval r = 0.4392 to 0.7744 inflammatory cytokines IL6 was able to strongly stimulate hepcidin expression and as consequence such indicator could be responsible for hypoferriemia accompanied with chronic inflammatory diseases,…”
BackgroundResultInfluentialHematologic manifestations of celiac disease
Kružliak, P. (2012) · InTech eBooks · doi:10.5772/31233 · Cited by 2
Canavesi, E., & Valenti, L. V. C. (2011) · InTech eBooks · doi:10.5772/22735 · Cited by 2
Paubelle, É., & Herbaux, C. (2013) · Hématologie · doi:10.1684/hma.2013.0805 · Cited by 2
Oliveras, A., & Espel, E. (2007) · Medical Hypotheses · doi:10.1016/j.mehy.2007.07.021 · Cited by 2
“The biosynthesis of this peptide by the liver is controlled mainly by the pro-inflammatory cytokine IL-6 [9], and presumably by iron hypoxia demands among others [10,11].”
BackgroundInterleukine-6 : de la dcouverte de la cytokine au dveloppement dun traitement cibl
Assier, E., Boissier, M., & Dayer, J. (2010) · Revue du Rhumatisme · doi:10.1016/s1169-8330(10)70004-1 · Cited by 2
Resistance to Recombinant Human Erythropoietin Therapy in Haemodialysis Patients
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Recombinant Expression of an Antimicrobial Peptide Hepcidin in Pichia pastoris
Rashid, F., Ali, I., Sajid, I., El‐Amin, S. F., & Yuan, Q. (2009) · Pakistan Journal of Zoology · Cited by 2
Tayebi, S. M., Mahdian, H., & Mahmoudi, S. A. (2016) · International Journal of Applied Exercise Physiology · Cited by 2
Assessment of Serum Iron and Zinc Status in Febrile Seizures – A Prospective Case Control Study
Joshi, S. S. (2014) · IOSR Journal of Dental and Medical Sciences · doi:10.9790/0853-131015189 · Cited by 2
Hematologic Complications of Chronic Kidney Disease
Berns, J. S. (2014) · Elsevier eBooks · doi:10.1016/b978-0-12-411602-3.00022-6 · Cited by 2
Anemia and Iron Deficiency in Heart Failure — Clinical Update
Mester, A., Mitre, A., Lázár, E., Benedek, I., Sándor-Kéri, J., Pakucs, A., & Benedek, I. (2017) · Journal of Interdisciplinary Medicine · doi:10.1515/jim-2017-0092 · Cited by 2
Monitoring Hepcidin Level in Chronic Hepatitis C Virus Patients during Therapy
Khadr, N., Okasha, H. A. S., Nouh, H. H., & Semary, W. (2014) · Afro-Egyptian Journal of Infectious and Endemic Diseases · doi:10.21608/aeji.2014.17201 · Cited by 2
“Hepcidin binds to the iron exporter ferroportin, which results in ferroportin internalization and degradation [13,14,15].”
BackgroundFerropenia sin anemia, más que un hallazgo de laboratorio
Arsanios, D. M., Serrano, S., Espinel, B., Quintero-Muñoz, E., Rincón, M. J. G., & Bastidas, A. (2018) · Universitas Médica · doi:10.11144/javeriana.umed59-4.ferr · Cited by 2
“La ERC produce disbalance en el metabolismo y absorción del hierro, la inflamación crónica lleva a la producción de citocinas y otros productos de la inflamación, en especial la IL-6 aumenta la producción de hepcidina a nivel hepático, disminuyendo así la absorción de hierro digestiva por inhibición de canales ferropo…”
BackgroundEffects of diet before endurance exercise on hepcidin response in young untrained females
Hayashi, N., Ishibashi, A., & Goto, K. (2018) · Physical Activity and Nutrition · doi:10.20463/jenb.2018.0030 · Cited by 2
Kovchun, A. V., Кміта, В. В., & Приступа, Л. Н. (2018) · Lviv clinical bulletin · doi:10.25040/lkv2018.04.033 · Cited by 2
Iron Deficiency Anaemia and Cancer
Bouri, S., & Martin, J. (2019) · Journal of Cancer Treatment and Diagnosis · doi:10.29245/2578-2967/2019/3.1167 · Cited by 2
Zou, L., Lu, M., Guo, L., Teng, L., Xu, Y., & Zheng, Q. (2017) · PubMed Central · doi:10.3785/j.issn.1008-9292.2017.08.12 · Cited by 2
Analysis of Natural Killer cell functions in patients with hereditary hemochromatosis
Bönnemann, V., Claus, M., Butzeck, B., Collette, D., Bröde, P., Golka, K., & Watzl, C. (2020) · EXCLI journal · doi:10.17179/excli2020-1116 · Cited by 2
Walczak, J., Hasan, S., Shoaee, N., Tromblay, D., & Muthumalaiappan, K. (2020) · Shock · doi:10.1097/shk.0000000000001649 · Cited by 2
“Unauthori been shown to stimulate the release of hepcidin from the liver, impeding the availability of iron in chronic inflammatory conditions causing anemia (21).”
BackgroundЕршов, В. И., Gadaev, I. Y., Соломахина, Н. И., Nakhodnova, E. S., & Сергеевна, К. Е. (2017) · Clinical Medicine (Russian Journal) · doi:10.18821/0023-2149-2017-95-10-869-874 · Cited by 2
Al-Abedy, N. M. M., Salman, E. D., & Faraj, S. A. (2021) · Indian Journal of Forensic Medicine & Toxicology · doi:10.37506/ijfmt.v15i3.15505 · Cited by 2
“(12) These results in ferrοpοrtin internalizatiοn and degradatiοn decreased the entry οf irοn intο the plasma cοmpartment.”
Gubkina, L. V., & Васильевна, С. А. (2021) · Siberian Journal of Life Sciences and Agriculture · doi:10.12731/2658-6649-2021-13-4-159-174 · Cited by 2
“Интерлейкин-6, регулируя экспрессию гипоталамических нейропептидов [18], считается главным супрессором иммунного ответа опухолевого микроокружения [19], а также является основным индуктором главного регулятора уровня железа – гепcидина [16].”
Touzot, M., Lefèbvre, T., Maheas, C., Peoc’h, K., Ureña, P., Ridel, C., Puy, H., & Karim, Z. (2021) · Clinical Kidney Journal · doi:10.1093/ckj/sfab254 · Cited by 2
“Here we additionally explored hepcidin, themaster regulator of iron homeostasis that has rarely been measured in COVID-19 and interleukin-6 (IL-6), the cytokine that stimulates hepcidin in inflammatory conditions [3].”
BackgroundMartin, N. M., von Hurst, P. R., Conlon, C. A., Smeele, R., Mugridge, O., & Beck, K. L. (2023) · Military Medicine · doi:10.1093/milmed/usad023 · Cited by 2
REDD1 deletion and treadmill running increase liver hepcidin and gluconeogenic enzymes in male mice
Barney, D. E., Gordon, B. S., & Hennigar, S. R. (2023) · Journal of Nutritional Science · doi:10.1017/jns.2023.37 · Cited by 2
“High concentrations of dietary iron have been shown to increase liver iron stores and mask the hepcidin response to iron-loading and inflammatory agents((41)), suggesting that the increase in hepcidin with exercise in the present study is robust.”
BackgroundBhattacharya, N. (2008) · Springer eBooks · doi:10.1007/978-1-84800-167-1_10 · Cited by 2
“iron-regulated acute-phase protein that is composed of 25 amino acids, has helped to shed light on the relationship of the immune response to iron homeostasis and anemia of chronic disease [ 41 , 42].”
Background2. Hepcidin: From Discovery to Differential Diagnosis.
Tomosugi, N. (2010) · Nihon Naika Gakkai Zasshi · doi:10.2169/naika.99.1180 · Cited by 2
Anti-Interleukin-6 Receptor Antibody Therapy Against Autoimmune Inflammatory Diseases
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Matsuo-Tezuka, Y., Noguchi‐Sasaki, M., Kurasawa, M., Yorozu, K., & Shimonaka, Y. (2017) · International Journal of Hematology · doi:10.1007/s12185-017-2215-3 · Cited by 2
Alamir, M. A., Hassan, A. A.-E. M., Elshafie, S. M., Elabdin, H. M. Z., & Taha, S. A. (2017) · The Egyptian Journal of Internal Medicine · doi:10.4103/ejim.ejim_28_17 · Cited by 2
Cross, J., Jarjou, O., Mohammed, N. I., Prentice, A. M., & Cerami, C. (2019) · Gates Open Research · doi:10.12688/gatesopenres.12963.2 · Cited by 2
“The host inflammatory mediators, IL6 26 , IL22 27 and Type 1 interferon 28 , have been found to increase transcription of hepcidin through several Toll-like receptor (TLR) ligands 29 and STAT3 signalling 30,31 resulting in decreased systemic iron concentrations in the circulation.”
BackgroundZeinivand, M., Nahavandi, A., Baluchnejadmojarad, T., Roghani, M., & Golab, F. (2019) · International Journal of Peptide Research and Therapeutics · doi:10.1007/s10989-019-09912-5 · Cited by 2
“During chronic inflammation, higher levels of hepcidin and IL-6 have been related to anemia of inflammation, a condition that prevents the release of iron from intracellular store (Nemeth et al. 2004).”
BackgroundIron-related immune cell function in sepsis
Thorburn, T. (2019) · DalSpace (Dalhousie University) · Cited by 2
Cui, Z., Tan, B., Liao, S., Qi, M., Wang, X., Zha, A., Kong, X., Chen, Y., & Liao, P. (2020) · BioMed Research International · doi:10.1155/2020/1475831 · Cited by 2
“It has been found that IL-6 can regulate inflammatory hypoxemia by inducing the synthesis of the iron-regulating hormone hepcidin [31].”
BackgroundTHE ROLE OF HEPCIDIN 25 IN THE DEVELOPMENT OF ANEMIC SYNDROME ASSOCIATED WITH MALIGNANT DISEASES
Назировна, Х. М., Владимирович, С. А., Blindar, V. N., Ryabchikov, D. A., Dobrovolskaya, M. M., Кононенко, И. Б., Kelemetov, A. M., Kazakov, A. M., & Palchinskaia, O. V. (2020) · Russian Journal of Biotherapy · doi:10.17650/1726-9784-2020-19-4-29-34 · Cited by 2
AFLATOKSİNLERİN ANNE VE ÇOCUK SAĞLIĞINA ETKİLERİ
Demirer, B., & Özdemir, M. T. (2021) · Kocatepe tıp dergisi. · doi:10.18229/kocatepetip.751953 · Cited by 2
Iron Status, Inflammation and Anemia in Bangladeshi Women Exposed to Arsenic
Faraj, J. M. (2023) · ScholarWorks@UMassAmherst (University of Massachusetts Amherst) · doi:10.7275/1696842 · Cited by 2
Evaluation and Management of Anemia in Older Individuals
Thomas, D. R., & Cepeda, O. A. (2006) · Aging Health · doi:10.2217/1745509x.2.2.303 · Cited by 2
Ironing out haemochromatosis : a study of an Indian family
Hallendorff, M.-A. (2008) · SUNScholar (Stellenbosch University) · Cited by 2
Suh, S. H., Oh, T. R., Choi, H. S., Kim, C. S., Bae, E. H., Kwon, S. S., Oh, K., Lee, K., Jung, J. Y., Kim, S. W., et al. (2024) · Kidney Diseases · doi:10.1159/000542057 · Cited by 2
Przybyszewska, J., & Żekanowska, E. (2014) · Annals of Agricultural and Environmental Medicine · doi:10.5604/1232-1966.1108600 · Cited by 2
“Interleukin-6 induces hepcidin expression, thus being a mediator in the development of hypoferremia [23, 24].”
BackgroundHepcydyna — hormon wątrobowy kontrolujący homeostazę żelaza
Filipczyk, L., Król, P., & Wystrychowski, A. (2010) · Via Medica Journals · Cited by 2
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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