Identification of erythroferrone as an erythroid regulator of iron metabolism
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Recovery from blood loss requires a greatly enhanced supply of iron to support expanded erythropoiesis. After hemorrhage, suppression of the iron-regulatory hormone hepcidin allows increased iron absorption and mobilization from stores. We identified a new hormone, erythroferrone (ERFE), that mediates hepcidin suppression during stress erythropoiesis. ERFE is produced by erythroblasts in response to erythropoietin. ERFE-deficient mice fail to suppress hepcidin rapidly after hemorrhage and exhibit a delay in recovery from blood loss. ERFE expression is greatly increased in Hbb(th3/+) mice with thalassemia intermedia, where it contributes to the suppression of hepcidin and the systemic iron overload characteristic of this disease.
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In iron-loading anemias, such as β-thalassemia, enhanced albeit ineffective erythropoiesis releases erythroferrone, which sequesters BMP receptor ligands, thereby inhibiting hepcidin.
“In iron-loading anemias, such as β-thalassemia, enhanced albeit ineffective ery-thropoiesis releases erythroferrone, which sequesters BMP receptor ligands, thereby inhibiting hepcidin.”
From Iron metabolism and iron disorders revisited in the hepcidin era (2020) · cites this paper as [52]
Erythroferrone (ERFE) is released by erythroid precursors stimulated by erythropoietin to suppress hepcidin expression and favor iron acquisition for hemoglobin synthesis.
“Erythroferrone (ERFE) is released by erythroid precursors stimulated by erythropoietin to suppress hepcidin expression and favor iron acquisition for hemoglobin synthesis.52”
From Iron metabolism and iron disorders revisited in the hepcidin era (2020) · cites this paper as [52]
Erythroferrone is produced by erythroblasts in response to erythropoietic stimulation and suppresses hepcidin synthesis, making more iron available for erythropoiesis.
“Another set of regulatory factors conveys the iron requirements for erythropoiesis and includes the recently identified hormone erythroferrone12, which is produced by erythroblasts in response to erythropoietic stimulation by endogenous or synthetic erythropoietin. Erythroferrone suppresses hepcidin synthesis, making more iron available for enhanced erythropoiesis.”
From Iron homeostasis in host defence and inflammation (2015) · cites this paper as [12]
In untransfused patients with β-thalassaemia, blood hepcidin levels are very low despite high iron concentrations and iron deposition, due to suppression by mediators from expanded erythroblasts.
“Despite high concentrations of iron and deposition of iron in the liver and other vital organs, the blood level of hepcidin in untransfused patients with β-thalassaemia is very low38–40, owing to suppression by mediators originating from the expanded erythroblast population in the bone marrow12,41.”
From Iron homeostasis in host defence and inflammation (2015) · cites this paper as [12]
Erythroferrone is produced by EPO-stimulation of erythroid progenitors and blocks hepcidin synthesis in hepatocytes.
“Erythroferrone (ERFE) is produced by erythropoietin (EPO)-stimulation of erythroid progenitors and blocks hepcidin synthesis in the hepatocytes (Kautz et al., 2014).”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Kautz et al., 2014
Hepcidin expression is repressed by hypoferremia, anemia, tissue hypoxia, and hormones such as GDF15, erythroferrone, PDGF-BB, and testosterone.
“and repressed in response to: (i) hypoferremia, that is, lower than normal levels of circulating Fe, (ii) anemia, (iii) tissue hypoxia, and (iv) hormones, for example, growth and differentiation factors 15, erythroferrone, platelet-derived growth factor-BB (PDGF-BB) and testosterone [62][63][64][65].”
From The Iron age of host–microbe interactions (2015) · cites this paper as [62]
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- Authors
- Kautz, L., Jung, G., Valore, E. V., Rivella, S., Nemeth, E., & Ganz, T.
- Affiliations
- University of California, Los Angeles (US)
- Weill Cornell Medicine (US)
- Corresponding author
- Ganz, Tomas
- Venue
- Nature Genetics
- Published
- 2014-06-01
- Volume
- 46
- Issue
- 7
- Pages
- 678-684
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC4104984
- OpenAlex
- W2006046265
- Cited by
- 1,127
- References
- 44
- Citations by year
- 2026: 60 · 2025: 76 · 2024: 63 · 2023: 88 · 2022: 81 · 2021: 116 · 2020: 111 · 2019: 94 · 2018: 109 · 2017: 107 · 2016: 92 · 2015: 101 · 2014: 27
- FWCI
- 72.77
- Type
- journal article
- Language
- en
- Update notices
- correction (2020-02-27)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Cancer Institute (CA-16 042, P30CA016042)
- National Institute of Allergy and Infectious Diseases (AI-28 697, P30AI028697)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK065029, R01DK090554, P30DK041301, R01DK095112)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Genetics › Hemoglobinopathies and Related Disorders
- Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
- Keywords
- erythroferrone, erythropoietin, hepcidin, iron metabolism, stress erythropoiesis, erythroblasts, beta-thalassemia, thalassemia intermedia, iron overload, iron absorption, iron mobilization, iron regulatory hormone
- MeSH terms
- Epoetin Alfa, Anemia, Animals, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Erythropoiesis, Erythropoietin, Hemoglobins, Hemorrhage, Hormones, Iron, Liver, Male, Mice, Inbred C57BL, Molecular Sequence Data, Recombinant Proteins, RNA, Messenger, Blotting, Western, beta-Thalassemia, Mice, Knockout, Iron Overload, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, Mice, Real-Time Polymerase Chain Reaction, Hepcidins
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