Hepcidin is suppressed by erythropoiesis in hemoglobin E β-thalassemia and β-thalassemia trait
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Key Points: Expanded erythropoiesis strongly drives hepcidin suppression in severe transfusion-dependent HbE β-thalassemia. β-thalassemia carriers, but not HbE carriers, have enhanced erythropoiesis associated with mildly suppressed hepcidin.
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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 [40]
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Effect of HFE Gene Mutations on Iron Metabolism of Beta-Thalassemia Carriers
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- Authors
- Jones, E., Pasricha, S.-R., Allen, A., Evans, P., Fisher, C. A., Wray, K., Premawardhena, A., Bandara, D., Perera, A., Webster, C., Sturges, P., Olivieri, N. F., St. Pierre, T., Armitage, A. E., Porter, J. B., Weatherall, D. J., & Drakesmith, H.
- Affiliations
- University of Oxford (GB)
- Swansea University (GB)
- University College London (GB)
- Medical Research Council, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom;
- University of Kelaniya (LK)
- National Hospital of Sri Lanka (LK)
- Heartlands Hospital (GB)
- University Health Network (CA)
- School of Physics, University of Western Australia, Crawley, Australia
- ORCID
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2015-01-29
- Volume
- 125
- Issue
- 5
- Pages
- 873-880
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC4321326
- OpenAlex
- W2001570896
- Cited by
- 68
- References
- 43
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 3 · 2023: 8 · 2022: 4 · 2021: 6 · 2020: 3 · 2019: 5 · 2018: 10 · 2017: 8 · 2016: 7 · 2015: 6
- FWCI
- 3.51
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- UWA Profiles and Research Repository (UWA) (submittedVersion, other-oa)
- Funders
- Bill and Melinda Gates Foundation
- March of Dimes Foundation
- Wellcome Trust
- NIHR Biomedical Research Centre, Royal Marsden NHS Foundation Trust/Institute of Cancer Research
- National Institute for Health and Care Research
- Haematology Society of Australia and New Zealand
- Medical Research Council
- National Health and Medical Research Council
- Topics
- Health Sciences › Medicine › Genetics › Hemoglobinopathies and Related Disorders
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hemoglobin structure and function
- Keywords
- hepcidin, erythropoiesis, HbE/β-thalassemia, beta-thalassemia trait, iron overload, iron accumulation, disease phenotypes, iron supplementation, anemia
- MeSH terms
- Adolescent, Adult, Carrier State, Child, Child, Preschool, Erythropoiesis, Female, Gene Expression Regulation, Genotype, Hemoglobin E, Humans, Iron, Male, Middle Aged, Mutation, Phenotype, Severity of Illness Index, Sri Lanka, Linear Models, Case-Control Studies, beta-Thalassemia, Iron Overload, beta-Globins, Hepcidins, Transfusion Reaction
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