ArticleThe Journal of clinical investigation2010
Hepcidin as a therapeutic tool to limit iron overload and improve anemia in β-thalassemic mice.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
134 citing papers in PubMed, 218 citations in OpenAlex.
- A variant erythroferrone disrupts iron homeostasis inScience translational medicine · 2019Trial
- Integrated protein quality-control pathways regulate free α-globin in murine β-thalassemia.Blood · 2012Trial
- Elevated liver iron concentration is a marker of increased morbidity in patients with β thalassemia intermedia.Haematologica · 2011Trial
- Urine hepcidin has additive value in ruling out cardiopulmonary bypass-associated acute kidney injury: an observational cohort study.Critical care (London, England) · 2011Trial
- Contemporary Management of Thalassemia: A Perspective on Current Standards and the Emergence of FDA-Approved Oral Therapy.Health science reports · 2026Article
- Multiomics analysis of red blood cells reveals thalassemia severity beyond globin gene mutations.Blood advances · 2026Article
- CCND3 Suppression Ameliorates β-Thalassaemia in a Murine Disease Model: A Potential Therapeutic Strategy.Cells · 2026Article
- Hepcidin mediates the disorder of iron homeostasis and mitochondrial function in mice under hypobaric hypoxia exposure.Apoptosis : an international journal on programmed cell death · 2025Article
- Three signalling pathways for iron overload in osteoporosis: a narrative review.Journal of orthopaedic surgery and research · 2025Review
- Iron-Loading Anemias.Advances in experimental medicine and biology · 2025Review
- Current Landscape of Hepcidin Therapeutics.Advances in experimental medicine and biology · 2025Review
- In vivo silencing of intestinal DMT1 mitigates iron loading in β-thalassemia intermedia (Hbbth3/+) mice.Blood advances · 2024Article
- Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects.Signal transduction and targeted therapy · 2024Review
- Article
- A human anti-matriptase-2 antibody limits iron overload, α-globin aggregates, and splenomegaly in β-thalassemic mice.Blood advances · 2024Article
- Effects of Thalidomide on Erythropoiesis and Iron Homeostasis in Transfusion-Dependent β-Thalassemia.Mediterranean journal of hematology and infectious diseases · 2024Article
- Erythroferrone exacerbates iron overload and ineffective extramedullary erythropoiesis in a mouse model of β-thalassemia.Blood advances · 2023Article
- Article
- (De)ironing out sickle cell disease.Blood · 2023Article
- Editorial: Stress erythropoiesis.Frontiers in physiology · 2023Article
74 more citing papers are in PubMed but not listed here.
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Authors and funding
19 authors at 5 institutions in 1 country.
Funding
Abstract
Excessive iron absorption is one of the main features of β-thalassemia and can lead to severe morbidity and mortality. Serial analyses of β-thalassemic mice indicate that while hemoglobin levels decrease over time, the concentration of iron in the liver, spleen, and kidneys markedly increases. Iron overload is associated with low levels of hepcidin, a peptide that regulates iron metabolism by triggering degradation of ferroportin, an iron-transport protein localized on absorptive enterocytes as well as hepatocytes and macrophages. Patients with β-thalassemia also have low hepcidin levels. These observations led us to hypothesize that more iron is absorbed in β-thalassemia than is required for erythropoiesis and that increasing the concentration of hepcidin in the body of such patients might be therapeutic, limiting iron overload. Here we demonstrate that a moderate increase in expression of hepcidin in β-thalassemic mice limits iron overload, decreases formation of insoluble membrane-bound globins and reactive oxygen species, and improves anemia. Mice with increased hepcidin expression also demonstrated an increase in the lifespan of their red cells, reversal of ineffective erythropoiesis and splenomegaly, and an increase in total hemoglobin levels. These data led us to suggest that therapeutics that could increase hepcidin levels or act as hepcidin agonists might help treat the abnormal iron absorption in individuals with β-thalassemia and related disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.