Novel Circulating Isoforms of Hepcidin

Moe, Morten K.; Hardang, Ingrid Marie M.; Hagve, Tor‐Arne

doi:10.1373/clinchem.2013.208371

Cited by 9 publications

(6 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…N-terminal degradation leads to smaller isoforms (hepcidin-24, -23, -22, and -20) of unknown significance. [7][8][9] These isoforms are generally present in diseases with elevated hepcidin-25 levels, including chronic kidney disease and sepsis. 10,11 Circulating hepcidin is bound to a-2-macroglobulin and albumin, but estimates of this binding vary from ,3% to 89% of total.…”

Section: Hepcidin Structure and Kineticsmentioning

confidence: 99%

Hepcidin in the diagnosis of iron disorders

Girelli

Nemeth

Swinkels

2016

Blood

346

291

View full text Add to dashboard Cite

The discovery of the iron-regulatory hormone hepcidin in 2001 has revolutionized our understanding of iron disorders, and its measurement should advance diagnosis/treatment of these conditions. Although several assays have been developed, a gold standard is still lacking, and efforts toward harmonization are ongoing. Nevertheless, promising applications can already be glimpsed, ranging from the use of hepcidin levels for diagnosing iron-refractory iron deficiency anemia to global health applications such as guiding safe iron supplementation in developing countries with high infection burden.

show abstract

Section: Hepcidin Structure and Kineticsmentioning

confidence: 99%

Hepcidin in the diagnosis of iron disorders

Girelli

Nemeth

Swinkels

2016

Blood

346

291

View full text Add to dashboard Cite

show abstract

“…After activation of the BMP receptor, the SMAD pathway is activated leading to over-expression of hepcidin. In contrast, hepcidin mRNA is suppressed in anemia [59], but this effect is probably indirect, depending on the erythropoietin production [60]. Furthermore, at least 3 other proteins play roles by interacting between BMPs and the BMP receptor.…”

Section: Hepcidin; the Queen Of ‘Ironomics'mentioning

confidence: 99%

“…Prohepcidin was found to specifically bind to the STAT3 site in the promoter of the HAMP gene, thus suggesting that prohepcidin affects the expression of its own gene, indicating an autoregulatory loop of hepcidin gene expression [24]. Using liquid chromatography in combination with high-resolution mass spectrometry, we and others were able to identify new forms of hepcidin in human plasma or serum samples [59,60]. …”

Section: Hepcidin; the Queen Of ‘Ironomics'mentioning

confidence: 99%

Physiology of Iron Metabolism

Waldvogel-Abramowski

Waeber²,

Gassner³

et al. 2014

Transfus Med Hemother

208

146

View full text Add to dashboard Cite

A revolution occurred during the last decade in the comprehension of the physiology as well as in the physiopathology of iron metabolism. The purpose of this review is to summarize the recent knowledge that has accumulated, allowing a better comprehension of the mechanisms implicated in iron homeostasis. Iron metabolism is very fine tuned. The free molecule is very toxic; therefore, complex regulatory mechanisms have been developed in mammalian to insure adequate intestinal absorption, transportation, utilization, and elimination. ‘Ironomics' certainly will be the future of the understanding of genes as well as of the protein-protein interactions involved in iron metabolism.

show abstract

“…Hepcidin binds to the cellular iron exporter ferroportin (FPN) located on the basolateral membrane of hepatocytes and enterocytes and in macrophages and thereby restrains iron from entering the blood circulation [1,5,10]. Hepcidin exists in several isoforms (hepcidin- 25, -24, -23, -22, -20, and -19) [18], but hepcidin-25 (Hep25) has the highest affinity for FPN, and it is this isoform that has a central role in iron regulation [19]. Hep25 synthesis in HH patients is downregulated causing excess FPN-mediated iron export and increased dietary iron uptake from enterocytes in the intestine and iron export from macrophages.…”

Section: Introductionmentioning

confidence: 99%

Cytokine and Gene Expression Profiling in Patients with <b><i>HFE</i></b>-Associated Hereditary Hemochromatosis according to Genetic Profile

et al. 2020

View full text Add to dashboard Cite

Background: Hemochromatosis gene (HFE)-associated hereditary hemochromatosis (HH) is characterized by downregulation of hepcidin synthesis, leading to increased intestinal iron absorption. Objectives: The objectives were to characterize and elucidate a possible association between gene expression profile, hepcidin levels, disease severity, and markers of inflammation in HFE-associated HH patients. Methods: Thirty-nine HFE-associated HH patients were recruited and assigned to 2 groups according to genetic profile: C282Y homozygotes in 1 group and patients with H63D, as homozygote or in combination with C282Y, in the other group. Eleven healthy first-time blood donors were recruited as controls. Gene expression was characterized from peripheral blood cells, and inflammatory cytokines and hepcidin-25 isoform were quantified in serum. Biochemical disease characteristics were recorded. Results: Elevated levels of interleukin 8 were observed in a significant higher proportion of patients than controls. In addition, compared to controls, gene expression of ζ-globin was significantly increased among C282Y homozygote patients, while gene expression of matrix metalloproteinase 8, and other neutrophil-secreted proteins, was significantly upregulated in patients with H63D. Conclusion: Different disease signatures may characterize HH patients according to their HFE genetic profile. Studies on larger populations, including analyses at protein level, are necessary to confirm these findings.

show abstract

Novel Circulating Isoforms of Hepcidin

Cited by 9 publications

References 5 publications

Hepcidin in the diagnosis of iron disorders

Hepcidin in the diagnosis of iron disorders

Physiology of Iron Metabolism

Cytokine and Gene Expression Profiling in Patients with <b><i>HFE</i></b>-Associated Hereditary Hemochromatosis according to Genetic Profile

Contact Info

Product

Resources

About