ArticleWorld journal of gastroenterology2008
Function of the hemochromatosis protein HFE: Lessons from animal models.
Article in World journal of gastroenterology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 48 citations in OpenAlex.
- Higher iron stores and the HFE 187C>G variant delay onset of peripheral neuropathy during combination antiretroviral therapy.PloS one · 2020Trial
- Efficacy and safety of deferasirox in non-thalassemic patients with elevated ferritin levels after allogeneic hematopoietic stem cell transplantation.Bone marrow transplantation · 2016Trial
- Hemochromatosis and Hepatic Complications: A Comprehensive Review of Molecular Mechanisms, Diagnostics, and Emerging Therapeutics.Current molecular medicine · 2026Review
- The Importance and Essentiality of Natural and Synthetic Chelators in Medicine: Increased Prospects for the Effective Treatment of Iron Overload and Iron Deficiency.International journal of molecular sciences · 2024Review
- Evidence That HFE H63D Variant Is a Potential Disease Modifier in Cluster Headache.Journal of molecular neuroscience : MN · 2022Article
- Iron, Copper, and Zinc Homeostasis: Physiology, Physiopathology, and Nanomediated Applications.Nanomaterials (Basel, Switzerland) · 2021Review
- New Era in the Treatment of Iron Deficiency Anaemia Using Trimaltol Iron and Other Lipophilic Iron Chelator Complexes: Historical Perspectives of Discovery and Future Applications.International journal of molecular sciences · 2021Review
- Leukocyte telomere length is associated with iron overload in male adults with hereditary hemochromatosis.Bioscience reports · 2020Observational
- Transferrin and H-ferritin involvement in brain iron acquisition during postnatal development: impact of sex and genotype.Journal of neurochemistry · 2020Article
- Iron at the Centre ofFrontiers in cellular and infection microbiology · 2018Review
- Efficacy and safety of iron-chelation therapy with deferoxamine, deferiprone, and deferasirox for the treatment of iron-loaded patients with non-transfusion-dependent thalassemia syndromes.Drug design, development and therapy · 2016Review
- Chronic hepatitis C and liver fibrosis.World journal of gastroenterology · 2014Review
- Knowledge building insights on biomarkers of arsenic toxicity to keratinocytes and melanocytes.Biomarker insights · 2012Article
- Hepcidin expression in iron overload diseases is variably modulated by circulating factors.PloS one · 2012Article
- Establishment of secondary iron overloaded mouse model: evaluation of cardiac function and analysis according to iron concentration.Pediatric cardiology · 2011Article
- Highly Elevated Serum Hepcidin in Patients with Acute Myeloid Leukemia prior to and after Allogeneic Hematopoietic Cell Transplantation: Does This Protect from Excessive Parenchymal Iron Loading?Advances in hematology · 2011Article
- Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson's, Huntington's, Alzheimer's, prions, bactericides, chemical toxicology and others as examples.Archives of toxicology · 2010Review
- [Osteoarthritis in hereditary metabolic diseases].Der Orthopade · 2010Article
- [Osteoarthritis in hereditary metabolic diseases].Zeitschrift fur Rheumatologie · 2010Review
- Iron metabolism in thalassemia and sickle cell disease.Mediterranean journal of hematology and infectious diseases · 2009Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hereditary hemochromatosis (HH) is caused by chronic hyperabsorption of dietary iron. Progressive accumulation of excess iron within tissue parenchymal cells may lead to severe organ damage. The most prevalent type of HH is linked to mutations in the HFE gene, encoding an atypical major histocompatibility complex class I molecule. Shortly after its discovery in 1996, the hemochromatosis protein HFE was shown to physically interact with transferrin receptor 1 (TfR1) and impair the uptake of transferrin-bound iron in cells. However, these findings provided no clue why HFE mutations associate with systemic iron overload. It was later established that all forms of HH result from misregulation of hepcidin expression. This liver-derived circulating peptide hormone controls iron efflux from duodenal enterocytes and reticuloendothelial macrophages by promoting the degradation of the iron exporter ferroportin. Recent studies with animal models of HH uncover a crucial role of HFE as a hepatocyte iron sensor and upstream regulator of hepcidin. Thus, hepatocyte HFE is indispensable for signaling to hepcidin, presumably as a constituent of a larger iron-sensing complex. A working model postulates that the signaling activity of HFE is silenced when the protein is bound to TfR1. An increase in the iron saturation of plasma transferrin leads to displacement of TfR1 from HFE and assembly of the putative iron-sensing complex. In this way, iron uptake by the hepatocyte is translated into upregulation of hepcidin, reinforcing the concept that the liver is the major regulatory site for systemic iron homeostasis, and not merely an iron storage depot.
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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.