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.”
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Therapeutic Opportunities for Hepcidin in Acute Care Medicine
Chawla, L. S., Beers-Mulroy, B., & Tidmarsh, G. F. (2019) · Critical Care Clinics · doi:10.1016/j.ccc.2018.11.014 · Cited by 28
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Molecular Mechanisms of Ferroptosis and Its Role in Viral Pathogenesis
Huang, R.-W., Wu, J., Ma, Y., & Kang, K. (2023) · Viruses · doi:10.3390/v15122373 · Cited by 26
Barney, D. E., Ippolito, J., Berryman, C. E., & Hennigar, S. R. (2022) · Journal of Nutrition · doi:10.1093/jn/nxac129 · Cited by 26
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The Role of Vitamin D in Anemia
Netting, M., Best, K. P., & Green, T. (2022) · Nutrition and health · doi:10.1007/978-3-031-14521-6_15 · Cited by 26
Rapid removal of phagosomal ferroportin in macrophages contributes to nutritional immunity
Flannagan, R. S., Farrell, T. J., Trothen, S. M., Dikeakos, J. D., & Heinrichs, D. E. (2021) · Blood Advances · doi:10.1182/bloodadvances.2020002833 · Cited by 25
“During infection, hepcidin, an acute phase protein, is upregulated in response to infection and inflammation, and the subsequent internalization of FPN contributes to the host Fe withholding response.(10) Given macrophages are important phagocytic cells that comprise part of the immediate antibacterial immune response…”
BackgroundIron Supplementation in Nephrology and Oncology: What Do We Have in Common?
Macdougall, I. C. (2011) · The Oncologist · doi:10.1634/theoncologist.2011-s3-25 · Cited by 25
BMP5 contributes to hepcidin regulation and systemic iron homeostasis in mice
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Serum pro‐hepcidin levels in term and preterm newborns with sepsis
Yapakçı, E., Tarcan, A., Çelik, B., Özbek, N. Y., & Gürakan, B. (2008) · Pediatrics International · doi:10.1111/j.1442-200x.2008.02688.x · Cited by 25
Witmer, C. M. (2013) · Pediatric Clinics of North America · doi:10.1016/j.pcl.2013.08.012 · Cited by 25
“Impaired iron hemostasis is secondary to cytokine stimulation of hepcidin.(22) As mentioned previously, hepcidin is a negative regulator of iron.”
BackgroundSerum levels of hepcidin and interleukin 6 in Parkinson’s disease
Kwiatek-Majkusiak, J., Geremek, M., Koziorowski, D., Tomasiuk, R., Szlufik, S., & Friedman, A. (2020) · Acta Neurobiologiae Experimentalis · doi:10.21307/ane-2020-026 · Cited by 25
“IL‑6 was shown to induce the secretion of hepcidin in mono‑ cytes and macrophages (Nemeth et al., 2003, 2004).”
BackgroundUnravelling the broader complexity of IL-6 involvement in health and disease
Jenkins, R. L., Hughes, S. T. O., Figueras, A. C., & Jones, S. A. (2021) · Cytokine · doi:10.1016/j.cyto.2021.155684 · Cited by 25
Wang, J., Sun, Q.-H., Zhang, J., Wang, H., & Liu, H. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23042019 · Cited by 24
“IL-6 has been shown to be a necessary and sufficient cytokine to induce hamp expression in mice, human hepatocytes, and cortical neurons [45,46].”
BackgroundThe prevalence and etiology of anemia among HIV-infected children in India
Shet, A., Arumugam, K., Rajagopalan, N., Dinakar, C., Krishnamurthy, S., Mehta, S., & Shet, A. S. (2011) · European Journal of Pediatrics · doi:10.1007/s00431-011-1599-y · Cited by 27
“Recently, investigators have elucidated the link between inflammatory cytokines and hepcidin by showing that IL-6 acts directly on hepatocytes to stimulate hepcidin production and subsequent hypoferremia in animal and human models [27].”
BackgroundEffects of Testosterone on Erythropoiesis in a Female Mouse Model of Anemia of Inflammation
Guo, W., Schmidt, P. J., Fleming, M. D., & Bhasin, S. (2016) · Endocrinology · doi:10.1210/en.2016-1150 · Cited by 25
“hepcidin expression (38, 39, 44, 45), which seem to match”
BackgroundInterplay between innate immunity and iron metabolism after acute pancreatitis
Chand, S. K., Singh, R. G., Pendharkar, S. A., Bharmal, S. H., & Petrov, M. S. (2017) · Cytokine · doi:10.1016/j.cyto.2017.09.014 · Cited by 25
The Role of Iron in Amyotrophic Lateral Sclerosis
Bu, X., Xiang, Y., & Guo, Y. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-981-13-9589-5_8 · Cited by 25
Medicinal signaling cells: A potential antimicrobial drug store
Khatibi, S. M. H., Kheyrolahzadeh, K., Barzegari, A., Saadat, Y. R., & Vahed, S. Z. (2020) · Journal of Cellular Physiology · doi:10.1002/jcp.29728 · Cited by 25
“esis is induced by different inflammation and infection stimuli such as inflammatory signals (IL‐6) (Ganz & Nemeth, 2012; Nemeth et al., 2004; Nicolas et al., 2002), LPS, Smad1/5/8, and activin B signaling in the liver (Besson‐Fournier et al.”
BackgroundInfluentialBhattacharya, N. (2006) · Malaria Journal · doi:10.1186/1475-2875-5-20 · Cited by 25
“The pathophysiology [7], iron metabolism [8,9] and erythropoietin production [10] in case of anemia in chronic disease is different.”
BackgroundMørkedal, B., Laugsand, L. E., Romundstad, P., & VATTEN, L. J. (2011) · European Journal of Cardiovascular Prevention & Rehabilitation · doi:10.1177/1741826710390134 · Cited by 25
“It is possible that low iron status is a late sign in the pathogenesis of IHD, such as a response to an inflammatory mechanism.(20) It is also possible that unknown but underlying disease could have influenced iron status and, therefore, the association with IHDmortality could be due to reverse causality.”
BackgroundEvaluation of standard liver volume formulae for Chinese adults
Shi, Z. (2009) · World Journal of Gastroenterology · doi:10.3748/wjg.15.4062 · Cited by 25
Lévesque, J.-P., SUMMERS, K. M., Bisht, K., Millard, S. M., Winkler, I. G., & Pettit, A. R. (2021) · Experimental Hematology · doi:10.1016/j.exphem.2021.08.011 · Cited by 26
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Iron overload and allogeneic hematopoietic stem-cell transplantation
Kanda, J., Kawabata, H., & Chao, N. J. A. (2011) · Expert Review of Hematology · doi:10.1586/ehm.10.81 · Cited by 25
Preoperative intravenous iron for anaemia in elective major open abdominal surgery: the PREVENTT RCT
Richards, T., Baikady, R. R., Clevenger, B., Butcher, A., Abeysiri, S., Chau, M., Swinson, R., Collier, T. J., Dodd, M., Dyck, L. V., et al. (2021) · Health Technology Assessment · doi:10.3310/hta25110 · Cited by 25
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Natural history of SLC11 genes in vertebrates: tales from the fish world
Neves, J. V., Wilson, J. M., Kuhl, H., Reinhardt, R., Castro, L. F. C., & Rodrigues, P. N. (2011) · BMC Evolutionary Biology · doi:10.1186/1471-2148-11-106 · Cited by 24
Duval, C., Macabiou, C., Garcia, C., Lesuisse, E., Camadro, J., & Auchère, F. (2019) · MicrobiologyOpen · doi:10.1002/mbo3.970 · Cited by 25
“Hepcidin plays a major role in lowering serum iron by inhibiting ferroportin, the mammalian iron-export protein (Donovan et al., 2005; Nemeth et al., 2004).”
BackgroundIron Supplementation Attenuates the Inflammatory Status of Anemic Piglets by Regulating Hepcidin
Pu, Y., Guo, B., Liu, D., Xiong, H., Wang, Y., & Du, H. (2015) · Biological Trace Element Research · doi:10.1007/s12011-015-0295-6 · Cited by 24
“During infection and inflammation, hepcidin synthesis is markly increased by a mechanism that is independent of iron status or erythropoietic activity [21].”
In vivo imaging of hepcidin promoter stimulation by iron and inflammation
Flanagan, J. M., Truksa, J., Peng, H., Lee, P. L., & Beutler, E. (2007) · Blood Cells Molecules and Diseases · doi:10.1016/j.bcmd.2007.01.004 · Cited by 24
“The regulation of hepcidin expression is thought to occur predominantly at the transcriptional level [4-6].”
BackgroundGarcia‐Manero, G., Gartenberg, G. J., Steensma, D. P., Schipperus, M. R., Breems, D. A., de Paz, R., Valcárcel, D., Kranenburg, B., Reddy, M. P., & Komrokji, R. S. (2014) · American Journal of Hematology · doi:10.1002/ajh.23780 · Cited by 24
“Moreover, increases in IL-6 have been shown to induce the synthesis of hepcidin during inflammation [8].”
BackgroundIL-6: A New Era for the Treatment of Autoimmune Inflammatory Diseases
Kishimoto, T., Kang, S., & Tanaka, T. (2015) · Springer eBooks · doi:10.1007/978-4-431-55651-0_11 · Cited by 24
Nienaber, A., Baumgartner, J., Dolman, R., Ozturk, M., Zandberg, L., Hayford, F. E. A., Brombacher, F., Blaauw, R., Parihar, S. P., Smuts, C. M., et al. (2020) · Nutrients · doi:10.3390/nu12092897 · Cited by 24
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“Nemeth E, Rivera S, Gabayan V, Keller C, Taudorf S, Pedersen BK, and Ganz T. IL-6 512 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin.”
BackgroundInfluentialSelf-citationWard, J. L., Torres‐Gonzalez, M., & Ammons, M. C. B. (2022) · Nutrients · doi:10.3390/nu14153090 · Cited by 24
“This treatment resulted in early viral clearance (15–30 days) along with decreases in IL-6, D-Dimer, and ferritin serum levels.”
BackgroundInfluentialHong, J. H., Choi, Y., Min, B.-K., Park, K. S., Seong, K., Lee, I. K., & Kim, J. G. (2015) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2015.05.001 · Cited by 24
“matory stimuli increase the level of the inflammatory cytokine IL-6 and then stimulate hepcidin expression in the liver [23,24].”
BackgroundChaudhury, C., Kim, J., Mehnaz, S., Wani, M. A., Oberyszyn, T. M., Bronson, C. L., Mohanty, S., Hayton, W. L., Robinson, J. M., & Anderson, C. L. (2006) · Journal of Nutrition · doi:10.1093/jn/136.12.2993 · Cited by 24
Bone marrow iron distribution, hepcidin, and ferroportin expression in renal anemia
Bârsan, L., Stanciu, A., Stancu, S. H., Căpuşă, C. S., Brătescu, L., Mandache, E., Radu, E., & Mircescu, G. (2015) · Hematology · doi:10.1179/1607845415y.0000000004 · Cited by 24
A seven day running training period increases basal urinary hepcidin levels as compared to cycling
Sim, M., DAWSON, B. T., Landers, G. J., Swinkels, D. W., Tjalsma, H., Wiegerinck, E. T. G., Trinder, D., & Peeling, P. (2014) · Journal of the International Society of Sports Nutrition · doi:10.1186/1550-2783-11-14 · Cited by 24
“levels degrade the ferroportin export channels on the surface of macrophages and the intestinal duodenum, resulting in a reduction in iron recycling (by macrophages from senescent erythrocytes) and absorption from the intestine, respectively [10,11].”
BackgroundSelenium, copper and iron in veterinary medicine—From clinical implications to scientific models
Humann‐Ziehank, E. (2016) · Journal of Trace Elements in Medicine and Biology · doi:10.1016/j.jtemb.2016.05.009 · Cited by 24
Humann‐Ziehank, E., Menzel, A., Röhrig, P., Schwert, B., Ganter, M., & Hennig‐Pauka, I. (2014) · Metallomics · doi:10.1039/c4mt00148f · Cited by 24
Laparra, J. M., Olivares, M., & Sanz, Y. (2013) · British Journal Of Nutrition · doi:10.1017/s0007114513001098 · Cited by 24
“In the initial phase of the inflammatory process, IL-6 is a key inducer of hepatic acute-phase protein synthesis, but also plays diverse biological activities in immune regulation, inflammation and haematopoiesis((6,41)).”
BackgroundMcCullough, P. A., Uhlig, K., Neylan, J. F., Pérgola, P. E., & Fishbane, S. N. (2018) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2018.04.062 · Cited by 24
Aguree, S., & Reddy, M. B. (2021) · Nutrients · doi:10.3390/nu13010217 · Cited by 24
“The accumulation and activation of macrophages release cytokines into the systemic circulation [24,25], particularly IL-6 (but also IL-1α and IL-1β), which stimulates hepatic hepcidin expression [39,40] and increased serum hepcidin concentration [27].”
BackgroundResultMaternal iron kinetics and maternal–fetal iron transfer in normal-weight and overweight pregnancy
Stoffel, N. U., Zimmermann, M. B., Cepeda-Lopez, A. C., Cervantes-Gracia, K., Llanas-Cornejo, D., Zeder, C., Tuntipopipat, S., Moungmaithong, S., Densupsoontorn, N., Lötscher, K. Q., et al. (2021) · American Journal of Clinical Nutrition · doi:10.1093/ajcn/nqab406 · Cited by 24
“Notably, despite higher inflammation in the OW group, including higher IL-6 [the main inducer of hepcidin during inflammation (39)], there were no group differences in maternal hepcidin over gestation, and inflammation was not a significant predictor of serum hepcidin (Table 2).”
BackgroundMoriconi, F., Ahmad, G., Ramadori, P., Malik, I. A., Sheikh, N., Merli, M., Riggio, O., Dudás, J., & Ramadori, G. P. (2009) · Laboratory Investigation · doi:10.1038/labinvest.2009.92 · Cited by 24
“41 Cytokine regulation of iron metabolism in hepatocytes has been reported previously”
BackgroundCoimbra, S., Catarino, C., Nascimento, H., Alves, A. I., Medeiros, A., Bronze-da-Rocha, E., Costa, E. M., Rocha‐Pereira, P., Aires, L., Seabra, A., et al. (2017) · Pediatric Research · doi:10.1038/pr.2017.139 · Cited by 25
Iron Status and Supplementation during Tuberculosis
Nienaber, A., Uyoga, M. A., Dolman, R., & Malan, L. (2023) · Microorganisms · doi:10.3390/microorganisms11030785 · Cited by 25
Stankiewicz, B., Cieślicka, M., Mieszkowski, J., Kochanowicz, A., Niespodziński, B., Szwarc, A., Waldziński, T., Reczkowicz, J., Piskorska, E., Petr, M., et al. (2023) · Nutrients · doi:10.3390/nu15040975 · Cited by 25
“However, there is increased data indicating that there is an interrelationship between oxidative stress, iron, inflammation, and skeletal muscle weakness and fatigue [4,9].”
BackgroundOlivari, V., Modica, S. M. D., Lidonnici, M. R., Aghajan, M., Cordero-Sánchez, C., Tanzi, E., Pettinato, M., Pagani, A., Tiboni, F., Silvestri, L., et al. (2023) · Kidney International · doi:10.1016/j.kint.2023.03.012 · Cited by 24
Anemia of Inflammatory, Neoplastic, Renal, and Endocrine Diseases
Grzelak, A. K., & Fry, M. M. (2022) · Wiley eBooks · doi:10.1002/9781119500537.ch39 · Cited by 24
A Strong Anti-Inflammatory Signature Revealed by Liver Transcription Profiling of Tmprss6-/- Mice
Riba, M., Rausa, M., Sorosina, M., Cittaro, D., Garcia Manteiga, J. M., Nai, A., Pagani, A., Martinelli-Boneschi, F., Stupka, E., Camaschella, C., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0069694 · Cited by 23
“Among them the anti-microbial peptide hepcidin, the main regulator of systemic iron homeostasis, is an acute phase protein expressed and secreted by the liver, which provides a critical connection with the immune response [2].”
BackgroundWang, K., Wu, J., Cheng, F., Huang, X. B., Zeng, F., & Zhang, Y. (2017) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2017/7601592 · Cited by 23
“As IL-6 is a primary driver for inflammation-inducible hepcidin expression in ACD [15], we next investigated whether ASP modified IL-6-induced 180”
BackgroundYamamoto, H., & Tsubakihara, Y. (2011) · Seminars in Dialysis · doi:10.1111/j.1525-139x.2011.00938.x · Cited by 23
“Anemia of chronic disease (ACD) has similar pathophysiologic mechanisms (14,15).”
BackgroundTocilizumab: molecular intervention therapy in children with systemic juvenile idiopathic arthritis
Yokota, S., & Kishimoto, T. (2010) · Expert Review of Clinical Immunology · doi:10.1586/eci.10.41 · Cited by 23
Püşüroğlu, H., Çakmak, H. A., Akgül, Ö., Ertürk, M., Sürgit, Ö., Akkaya, E., Bulut, Ü., & Yildirim, A. (2015) · Revista Portuguesa de Cardiologia · doi:10.1016/j.repc.2015.03.014 · Cited by 23
“Inflammation might contribute to increased RDW by inhibiting erythropoietin-induced erythrocyte maturation and impairing iron metabolism.(44,45) Furthermore, raised RDW may reflect the production of humoral mediators by bone marrow.”
BackgroundStallmach, A., & Büning, C. (2015) · Expert Opinion on Pharmacotherapy · doi:10.1517/14656566.2015.1096929 · Cited by 23
“Intestinal inflammation can be a contributory factor in the development of iron deficiency as it increases serum levels of interleukin-6 and this stimulates the synthesis of hepcidin, a peptide that plays a key role in iron homeostasis [3-5].”
BackgroundBella, L. M. D., Alampi, R., Biundo, F., Toscano, G., & Felice, M. R. (2017) · BMC Biochemistry · doi:10.1186/s12858-017-0076-2 · Cited by 23
“IL-6 was able to induce transcription of HAMP as previously reported [44], while the presence of BCS did not affect its expression level (Fig.”
BackgroundResultInfluentialEvaluation of serum hepcidin and iron levels in patients with PCOS: a case-control study
Rashidi, B. H., Shams, S., Shariat, M., Jaliseh, H. K., Mohebi, M., & Haghollahi, F. (2017) · Journal of Endocrinological Investigation · doi:10.1007/s40618-017-0632-z · Cited by 23
Ambachew, S., & Biadgo, B. (2017) · Acta Haematologica · doi:10.1159/000481391 · Cited by 23
Az albumin prognosztikai jelentősége az onkológiában
Deme, D., & Telekes, A. (2018) · Orvosi Hetilap · doi:10.1556/650.2018.30885 · Cited by 23
Nakayama, S., Matsuda, M., Adachi, T., Sueda, S., Ohashi, Y., Awaji, S., Hashimoto, S., & Matsumura, I. (2018) · Platelets · doi:10.1080/09537104.2018.1499889 · Cited by 23
Cui, J., Guo, X., Li, Q., Song, N., & Xie, J. (2020) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2020.00047 · Cited by 23
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Dose-dependent induction of IL-6 by plant-derived proteasesin vitro
Rose, B., Herder, C., Löffler, H., Meierhoff, G., Schloot, N. C., Walz, M., & Martin, S. (2005) · Clinical & Experimental Immunology · doi:10.1111/j.1365-2249.2005.02970.x · Cited by 23
Normal erythropoiesis but severe polyposis and bleeding anemia in Smad4-deficient mice
Pan, D., Schomber, T., Kalberer, C. P., Terracciano, L., Hafen, K., Krenger, W., Hao-Shen, H., Deng, C., & Skoda, R. C. (2007) · Blood · doi:10.1182/blood-2007-02-074393 · Cited by 23
Kanda, J., Mizumoto, C., Kawabata, H., Ichinohe, T., Tsuchida, H., Tomosugi, N., Matsuo, K., Yamashita, K., Kondo, T., Ishikawa, T., et al. (2009) · Transplantation and Cellular Therapy · doi:10.1016/j.bbmt.2009.04.008 · Cited by 23
“Hepatic expression of hepcidin can be upregulated by iron loading [16,17] as well as by inflammatory stimuli such as interleukin-6 (IL-6) [18].”
BackgroundThe role of iron supplementation during epoietin treatment for cancer-related anemia
Hedenus, M., & Birgegård, G. (2008) · Medical Oncology · doi:10.1007/s12032-008-9072-0 · Cited by 23
“It has been shown that chemotherapy increases endogenous serum levels of EPO [62] which can affect hepcidin levels, as can increased serum iron levels induced by RBC transfusions [ 63 ].”
BackgroundHow should hyperferritinaemia be investigated and managed?
Ong, S. Y., Nicoll, A., & Delatycki, M. B. (2016) · European Journal of Internal Medicine · doi:10.1016/j.ejim.2016.05.014 · Cited by 24
Hepcidin in chronic kidney disease anemia
Santos‐Silva, A., Ribeiro, S., Reis, F., & Belo, L. (2019) · Vitamins and hormones · doi:10.1016/bs.vh.2019.01.012 · Cited by 23
Pathophysiology of Iron Homeostasis during Inflammatory States
Cherayil, B. J. (2015) · The Journal of Pediatrics · doi:10.1016/j.jpeds.2015.07.015 · Cited by 24
“Subsequent experiments have confirmed IL-6-dependent up-regulation of hepcidin in mouse models of inflammatory bowel disease (IBD) and systemic bacterial, viral and parasitic infection (16-18).”
BackgroundInfluentialOgawa, C., Tsuchiya, K., Tomosugi, N., Kanda, F., Maeda, K., & Maeda, T. (2017) · PLoS ONE · doi:10.1371/journal.pone.0179608 · Cited by 23
An observational and Mendelian randomisation study on iron status and sepsis
Hamilton, F., Mitchell, R. E., Ahmed, H., Ghazal, P., & Timpson, N. J. (2023) · Scientific Reports · doi:10.1038/s41598-023-29641-6 · Cited by 23
Qin, X., Wu, P. S., Wen, T., Jia, R., Zhang, R., Jin, J., Hu, F., Chen, Q. Y., & Dang, J. (2022) · NeuroToxicology · doi:10.1016/j.neuro.2022.01.003 · Cited by 23
Elisio, C. (2014) · Aging and Disease · doi:10.14336/ad.2014.0500356 · Cited by 23
Carvalho, F., Medeiros, I., & Antunes, H. (2017) · Scandinavian Journal of Gastroenterology · doi:10.1080/00365521.2017.1342137 · Cited by 22
“All of these associated with increased requirements during growth explains a tendency to iron deficiency [2,8,11,21].”
BackgroundNahon, P., Charnaux, N., Friand, V., Prost‐Squarcioni, C., Ziol, M., Lievre, N., Trinchet, J., Beaugrand, M., Gattegno, L., Pessayre, D., et al. (2008) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2008.08.011 · Cited by 22
Molecular regulation of hepatic expression of iron regulatory hormone hepcidin
Oates, P. S., & Ahmed, U. (2007) · Journal of Gastroenterology and Hepatology · doi:10.1111/j.1440-1746.2007.04950.x · Cited by 22
Beigel, F., Löhr, B., Laubender, R. P., Tillack, C., Schnitzler, F., Breiteneicher, S., Weidinger, M., Göke, B., Seiderer, J., Ochsenkühn, T., et al. (2011) · Digestion · doi:10.1159/000333091 · Cited by 22
Hepcidin and its role in inflammatory bowel disease.
Dudkowiak, R., Neubauer, K., & Poniewierka, E. (2013) · PubMed · Cited by 22
Hepcidin discriminates sepsis from other critical illness at admission to intensive care
Olinder, J., Börjesson, A., Norrman, J., West, T., Carlström, J., Gustafsson, A., Annborn, M., Herwald, H., & Rydèn, C. (2022) · Scientific Reports · doi:10.1038/s41598-022-18826-0 · Cited by 22
A closer look at the role of iron in glioblastoma
Shenoy, G., & Connor, J. R. (2023) · Neuro-Oncology · doi:10.1093/neuonc/noad136 · Cited by 22
Identification, characterization and expression analysis of hepcidin gene in sheep
Badial, P. R., Oliveira-Filho, J. P., da Cunha, P. H. J., Cagnini, D. Q., Araújo, J. P., Winand, N. J., & Borges, A. S. (2010) · Research in Veterinary Science · doi:10.1016/j.rvsc.2010.07.017 · Cited by 23
“In humans, stimulation of the synthesis of hepcidin by IL-6 is accompanied by hypoferremia and decreased transferrin saturation (Nemeth et al., 2004a).”
BackgroundInfluentialBiological responses to spider silk-antibiotic fusion protein
Gomes, S. C. V., Gallego‐Llamas, J., Leonor, I. B., Mano, J. F., Reis, R. L., & Kaplan, D. L. (2011) · Journal of Tissue Engineering and Regenerative Medicine · doi:10.1002/term.437 · Cited by 23
“inflammation in mice and humans (Nemeth et al., 2004).”
Hepcidin as a potential biomarker for blood doping
Leuenberger, N., Bulla, E. G., Salamin, O., Nicoli, R., Robinson, N., Baume, N., & Saugy, M. (2016) · Drug Testing and Analysis · doi:10.1002/dta.2122 · Cited by 22
Planutis, A., Li, X., Trainor, C. D., Dangeti, M., Gillinder, K. R., Siatecka, M., Nébor, D., Peters, L. L., Perkins, A. C., & Bieker, J. J. (2017) · Development · doi:10.1242/dev.145656 · Cited by 22
“In the present case, the levels of hepcidin in the Nan/+ mouse are high enough to exert a physiological effect (Nemeth et al., 2004b).”
BackgroundMaretty‐Kongstad, K., Pedersen, N. A., Keller, J. O., & Safwat, A. (2017) · Translational Oncology · doi:10.1016/j.tranon.2017.09.002 · Cited by 22
Pavese, I., Satta, F., Todi, F., Palma, M. D., Piergrossi, P., Migliore, A., Piselli, P., Borghesi, R., Mancino, G., Brunetti, E., et al. (2009) · Annals of Oncology · doi:10.1093/annonc/mdp568 · Cited by 22
“Hepcidin is a regulator of iron metabolism and inhibits iron absorption and recycling from erythrophagocytosis by macrophages [21].”
BackgroundSalama, M., Bayele, H. K., & Srai, S. K. (2012) · Journal of Biomedical Science · doi:10.1186/1423-0127-19-83 · Cited by 22
“To better understand the biology of this, a study showed that humans injected with bacterial lipopolysaccharide (LPS) produced IL-6 within 3 hours, with concomitant increases in circulating hepcidin, and resulting in hypoferremia and reduced serum iron; similar findings were made in humans injected with IL-6 [20,21].”
BackgroundKhalil, S. K. M., Amer, H. A., EL-Behairy, A. M., & Warda, M. (2016) · Journal of Advanced Research · doi:10.1016/j.jare.2016.02.004 · Cited by 22
“[42], who illustrated that proinflammatory cytokines, mainly IL-6, negatively affect iron metabolism by stimulating the synthesis of hepcidin.”
BackgroundElsewefy, D. A., Farweez, B. A. T., Behairy, M., & Yassin, N. R. (2019) · International Urology and Nephrology · doi:10.1007/s11255-018-2062-z · Cited by 22
“[36] who demonstrated that IL-6 played a role in increasing the 0 20 40 60 80 100 Erythropoietin resistance index”
BackgroundUpregulation of Local Hepcidin Contributes to Iron Accumulation in Alzheimer’s Disease Brains
Chaudhary, S., Ashok, A., McDonald, D., Wise, A. S., Kritikos, A. E., Rana, N. A., Harding, C. V., & Singh, N. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210221 · Cited by 23
The Association between Hepcidin and Iron Status in Children and Adolescents with Obesity
Panichsillaphakit, E., Suteerojntrakool, O., Pancharoen, C., Nuchprayoon, I., & Chomtho, S. (2021) · Journal of Nutrition and Metabolism · doi:10.1155/2021/9944035 · Cited by 23
“(e releases of these cytokines mainly result in the release of hepcidin from the liver or adipose tissues [13].”
BackgroundNormal systemic iron homeostasis in mice with macrophage-specific deletion of transferrin receptor 2
Rishi, G., Secondes, E. S., Wallace, D. F., & Subramaniam, V. N. (2016) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00291.2015 · Cited by 21
“This increase in HAMP is thought to be mediated by the production of IL-6 by macrophages, which then acts through the JAK-STAT pathway resulting in the production of HAMP (22, 23, 41).”
BackgroundResultInfluentialRaha, A. A., Ghaffari, S. D., Henderson, J. W., Chakraborty, S., Allinson, K. S. J., Friedland, R. P., Holland, A. J., Zaman, S. H., Mukaetova-Ladinska, E. B., & Raha‐Chowdhury, R. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.653591 · Cited by 21
Iron Pathophysiology in Stroke
Almutairi, M. M., Xu, G., & Shi, H. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-981-13-9589-5_6 · Cited by 21
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
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