ReviewSeminars in liver disease2005
Pathophysiology of hereditary hemochromatosis.
Review in Seminars in liver disease, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Systemic review of genetic and epigenetic factors underlying differential toxicity to environmental lead (Pb) exposure.Environmental science and pollution research international · 2022Pooled it
- Comparing the types of haemochromatosis- from genetics to clinics.European journal of human genetics : EJHG · 2026Review
- Wheat landraces and microbiome endophytic phytases: In vitro/in silico study for iron bioavailability.Food chemistry. Molecular sciences · 2026Article
- Extracellular Vesicles as Biomarkers in Chronic Hepatobiliary Diseases: An Overview of Their Interplay.International journal of molecular sciences · 2025Review
- Oral iron therapy: Current concepts and future prospects for improving efficacy and outcomes.British journal of haematology · 2024Review
- Advances in CRISPR-Cas technology and its applications: revolutionising precision medicine.Frontiers in genome editing · 2024Review
- Sex differences in chronic liver disease and benign liver lesions.JHEP reports : innovation in hepatology · 2023Review
- Iron Metabolism: An Under Investigated Driver of Renal Pathology in Lupus Nephritis.Frontiers in medicine · 2021Review
- Article
- Hepatic Deficiency of Augmenter of Liver Regeneration Exacerbates Alcohol-Induced Liver Injury and Promotes Fibrosis in Mice.PloS one · 2016Article
- SLC39A14 Is Required for the Development of Hepatocellular Iron Overload in Murine Models of Hereditary Hemochromatosis.Cell metabolism · 2015Article
- The oral iron chelator deferiprone protects against systemic iron overload-induced retinal degeneration in hepcidin knockout mice.Investigative ophthalmology & visual science · 2014Article
- Article
- Loss of Hfe leads to progression of tumor phenotype in primary retinal pigment epithelial cells.Investigative ophthalmology & visual science · 2013Article
- Iron-mediated retinal degeneration in haemojuvelin-knockout mice.The Biochemical journal · 2012Article
- Polarized distribution of heme transporters in retinal pigment epithelium and their regulation in the iron-overload disease hemochromatosis.Investigative ophthalmology & visual science · 2011Article
- Iron regulation of hepcidin despite attenuated Smad1,5,8 signaling in mice without transferrin receptor 2 or Hfe.Gastroenterology · 2011Article
- Expression and iron-dependent regulation of succinate receptor GPR91 in retinal pigment epithelium.Investigative ophthalmology & visual science · 2011Article
- Expression and function of iron-regulatory proteins in retina.IUBMB life · 2010Review
- Absence of iron-regulatory protein Hfe results in hyperproliferation of retinal pigment epithelium: role of cystine/glutamate exchanger.The Biochemical journal · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Hereditary hemochromatosis (HH) encompasses several inherited disorders of iron homeostasis characterized by increased gastrointestinal iron absorption and tissue iron deposition. The most common form of this disorder is HFE-related HH, nearly always caused by homozygosity for the C282Y mutation. A substantial proportion of C282Y homozygotes do not develop clinically significant iron overload, suggesting roles for environmental factors and modifier genes in determining the phenotype. Recent studies have demonstrated that the pathogenesis of nearly all forms of HH involves inappropriately decreased expression of the iron-regulatory hormone hepcidin. Hepcidin serves to decrease the export of iron from reticuloendothelial cells and absorptive enterocytes. Thus, HH patients demonstrate increased iron release from these cell types, elevated circulating iron, and iron deposition in vulnerable tissues. The mechanism by which HFE influences hepcidin expression is an area of current investigation and may offer insights into the phenotypic variability observed in persons with mutations in HFE.
Indexed as
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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.