ReviewNature reviews. Disease primers2018
Haemochromatosis.
Review in Nature reviews. Disease primers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 226 papers, 4 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
226 citing papers in PubMed, 4 syntheses or guidelines pooled it, 388 citations in OpenAlex.
- Novel loci and biomedical consequences of iron homoeostasis variation.Communications biology · 2024Pooled it
- [Chinese guidelines for the diagnosis and treatment of hereditary hemochromatosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2024Guideline
- Clinical practice guidelines on hemochromatosis: Asian Pacific Association for the Study of the Liver.Hepatology international · 2023Guideline
- Iron Status and NAFLD among European Populations: A Bidirectional Two-Sample Mendelian Randomization Study.Nutrients · 2022Pooled it
- A phase 1b randomised clinical trial evaluating BBI-001, a non-absorbed oral therapeutic for the treatment of iron overload.Scientific reports · 2025Trial
- The effect of a natural polyphenol supplement on iron absorption in adults with hereditary hemochromatosis.European journal of nutrition · 2022Trial
- DDR1 sustains ferroptosis resistance in pancreatic ductal adenocarcinoma via SLC40A1-mediated iron homeostasis.Oncogene · 2026Article
- Cuproptosis in iron overload hepatocytes.Cell death & disease · 2026Article
- One Clinical Picture, Two Clinical Entities: A Case Report and Literature Review of Neurofibromatosis and Hemochromatosis.Children (Basel, Switzerland) · 2026Article
- Exploring the dynamics of FGF23 in patients with Hereditary Hemochromatosis type I following iron depletive treatment: a pilot study.Journal of endocrinological investigation · 2026Article
- Article
- TPC1-dependent control of endosomal pH and transferrin uptake determines cellular iron status.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Iron overload cardiomyopathy.Heart failure reviews · 2026Review
- Iron as a Key Mediator of Chronic Joint Damage: Insights from Hemophilic Arthropathy and Implications for Osteoarthritis.Medicina (Kaunas, Lithuania) · 2026Review
- Iron-addicted colorectal cancers exploit heme-complex II axis to resist oxidative cell death.Cell metabolism · 2026Article
- Comparing the types of haemochromatosis- from genetics to clinics.European journal of human genetics : EJHG · 2026Review
- Iron Overload: Pathophysiology, Diagnosis and Monitoring.International journal of laboratory hematology · 2026Review
- Ferroportin at the Crossroads of Iron Biology: Disease, Regulation and Modulation.Biomolecules · 2026Review
- Iron overload suppresses LKB1 and induces IL36G anti-tumor immunity in PDAC metastasis.Science advances · 2026Article
- Hepcidin as a Molecular Hub of Iron Homeostasis: From BMP-SMAD Signaling to Therapeutic Modulation.Biomolecules · 2026Review
166 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 4 countries.
Funding
Abstract
Haemochromatosis is defined as systemic iron overload of genetic origin, caused by a reduction in the concentration of the iron regulatory hormone hepcidin, or a reduction in hepcidin-ferroportin binding. Hepcidin regulates the activity of ferroportin, which is the only identified cellular iron exporter. The most common form of haemochromatosis is due to homozygous mutations (specifically, the C282Y mutation) in HFE, which encodes hereditary haemochromatosis protein. Non-HFE forms of haemochromatosis due to mutations in HAMP, HJV or TFR2 are much rarer. Mutations in SLC40A1 (also known as FPN1; encoding ferroportin) that prevent hepcidin-ferroportin binding also cause haemochromatosis. Cellular iron excess in HFE and non-HFE forms of haemochromatosis is caused by increased concentrations of plasma iron, which can lead to the accumulation of iron in parenchymal cells, particularly hepatocytes, pancreatic cells and cardiomyocytes. Diagnosis is noninvasive and includes clinical examination, assessment of plasma iron parameters, imaging and genetic testing. The mainstay therapy is phlebotomy, although iron chelation can be used in some patients. Hepcidin supplementation might be an innovative future approach.
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What OpenQuestion holds
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.