ArticleThe Journal of clinical investigation2011
Minihepcidins are rationally designed small peptides that mimic hepcidin activity in mice and may be useful for the treatment of iron overload.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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
119 citing papers in PubMed, 1 synthesis or guideline pooled it, 229 citations in OpenAlex.
- Pooled it
- Targeting the hepcidin-ferroportin pathway in anaemia of chronic kidney disease.British journal of clinical pharmacology · 2019Trial
- Hepcidin level predicts hemoglobin concentration in individuals undergoing repeated phlebotomy.Haematologica · 2013Trial
- Iron Homeostasis and Liver Diseases.Journal of cellular and molecular medicine · 2026Review
- Ferroportin at the Crossroads of Iron Biology: Disease, Regulation and Modulation.Biomolecules · 2026Review
- Hepcidin as a Molecular Hub of Iron Homeostasis: From BMP-SMAD Signaling to Therapeutic Modulation.Biomolecules · 2026Review
- Intestine-Specific Ferroportin Ablation Rescues from Systemic Iron Overload in Mice.Nutrients · 2026Article
- Genetic Engineering in Hematopoietic Stem Cells for β-Hemoglobinopathies Treatment: Advances, Challenges, and Clinical Translation.International journal of hematology-oncology and stem cell research · 2025Review
- Beyond blood transfusions: exploring iron chelation therapies in transfusion-dependent beta-thalassemia.Annals of medicine and surgery (2012) · 2025Article
- Cardiac injury caused by iron overload in thalassemia.Frontiers in pediatrics · 2025Review
- Role of Ferroptosis in ALD: Focusing on Hepcidin and Besides Hepcidin.Current medicinal chemistry · 2025Review
- The relationship between ghrelin and iron metabolism in beta thalassaemia major patients.Archives of medical science : AMS · 2025Article
- Current Landscape of Hepcidin Therapeutics.Advances in experimental medicine and biology · 2025Review
- Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects.Signal transduction and targeted therapy · 2024Review
- In vitro reconstitution of transition metal transporters.The Journal of biological chemistry · 2024Review
- Characterization and Clinical Assessment of a Peculiar Case of Hemolytic Anemia.Journal of hematology · 2024Article
- Iron Dysregulation in Cardiovascular Diseases.Reviews in cardiovascular medicine · 2024Review
- Iron metabolism and chronic inflammation in IgA nephropathy.Renal failure · 2023Review
- In vivo bioluminescence imaging of labile iron in xenograft models and liver using FeAL-1, an iron-activatable form of D-luciferin.Cell chemical biology · 2023Article
- The iron chaperone poly(rC)-binding protein 1 regulates iron efflux through intestinal ferroportin in mice.Blood · 2023Article
59 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Iron overload is the hallmark of hereditary hemochromatosis and a complication of iron-loading anemias such as β-thalassemia. Treatment can be burdensome and have significant side effects, and new therapeutic options are needed. Iron overload in hereditary hemochromatosis and β-thalassemia intermedia is caused by hepcidin deficiency. Although transgenic hepcidin replacement in mouse models of these diseases prevents iron overload or decreases its potential toxicity, natural hepcidin is prohibitively expensive for human application and has unfavorable pharmacologic properties. Here, we report the rational design of hepcidin agonists based on the mutagenesis of hepcidin and the hepcidin-binding region of ferroportin and computer modeling of their docking. We identified specific hydrophobic/aromatic residues required for hepcidin-ferroportin binding and obtained evidence in vitro that a thiol-disulfide interaction between ferroportin C326 and the hepcidin disulfide cage may stabilize binding. Guided by this model, we showed that 7–9 N-terminal amino acids of hepcidin, including a single thiol cysteine, comprised the minimal structure that retained hepcidin activity, as shown by the induction of ferroportin degradation in reporter cells. Further modifications to increase resistance to proteolysis and oral bioavailability yielded minihepcidins that, after parenteral or oral administration to mice, lowered serum iron levels comparably to those after parenteral native hepcidin. Moreover, liver iron concentrations were lower in mice chronically treated with minihepcidins than those in mice treated with solvent alone. Minihepcidins may be useful for the treatment of iron overload 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.