ArticleCell metabolism2009
Interaction of the hereditary hemochromatosis protein HFE with transferrin receptor 2 is required for transferrin-induced hepcidin expression.
Article in Cell metabolism, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers.
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Who cites it
164 citing papers in PubMed, 315 citations in OpenAlex.
- The neogenin-hemojuvelin axis in murine liver is crucial for hepcidin expression.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Red Blood Cell Distribution Width Is a Biomarker of Red Cell Dysfunction Associated with Inflammation, Macrophage Polarization, and Coronary Artery Calcification: A Prognostic Marker in Cardiovascular Disease and a Potential Target for Anti-Cytokine Therapy.Life (Basel, Switzerland) · 2026Review
- Comparing the types of haemochromatosis- from genetics to clinics.European journal of human genetics : EJHG · 2026Review
- Potential Usefulness of Urinary Hepcidin Measurement for Iron Deficiency Anemia in Female Athletes.European journal of sport science · 2026Article
- TFR2 p.A75V mutation aggravates liver iron overload in alcoholic liver disease via ERK pathway.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Iron, the Essential Micronutrient: A Comprehensive Review of Regulatory Pathways of Iron Metabolism.Nutrients · 2025Review
- Adipocytes orchestrate obesity-related chronic inflammation through β2-microglobulin.Signal transduction and targeted therapy · 2025Article
- Molecular Mechanisms of Iron Metabolism and Overload.Biomedicines · 2025Review
- HFE-Related Hemochromatosis May Be a Primary Kupffer Cell Disease.Biomedicines · 2025Review
- The role of redox-active iron, copper, manganese, and redox-inactive zinc in toxicity, oxidative stress, and human diseases.EXCLI journal · 2025Review
- Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects.Signal transduction and targeted therapy · 2024Review
- Red Blood Cell Distribution Width is a Biomarker of Red Cell Dysfunction Associated with High Systemic Inflammation and a Prognostic Marker in Heart Failure and Cardiovascular Disease: A Potential Predictor of Atrial Fibrillation Recurrence.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2024Review
- Mechanisms controlling cellular and systemic iron homeostasis.Nature reviews. Molecular cell biology · 2024Review
- Breaking the Barriers of Therapy Resistance: Harnessing Ferroptosis for Effective Hepatocellular Carcinoma Therapy.Journal of hepatocellular carcinoma · 2024Review
- Red Blood Cell Distribution Width as a Biomarker of Red Cell Dysfunction Associated with Inflammation and Macrophage Iron Retention: A Prognostic Marker in Heart Failure and a Potential Predictor for Iron Replacement Responsiveness.Cardiac failure review · 2024Article
- Review
- Liver Iron Loading in Alcohol-Associated Liver Disease.The American journal of pathology · 2023Review
- Overview of Ankle Arthropathy in Hereditary Hemochromatosis.Medical sciences (Basel, Switzerland) · 2023Review
- Managing the Dual Nature of Iron to Preserve Health.International journal of molecular sciences · 2023Review
- Article
104 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The mechanisms that allow the body to sense iron levels in order to maintain iron homeostasis are unknown. Patients with the most common form of hereditary iron overload have mutations in the hereditary hemochromatosis protein HFE. They have lower levels of hepcidin than unaffected individuals. Hepcidin, a hepatic peptide hormone, negatively regulates iron efflux from the intestines into the blood. We report two hepatic cell lines, WIF-B cells and HepG2 cells transfected with HFE, where hepcidin expression responded to iron-loaded transferrin. The response was abolished when endogenous transferrin receptor 2 (TfR2) was suppressed or in primary hepatocytes lacking either functional TfR2 or HFE. Furthermore, transferrin-treated HepG2 cells transfected with HFE chimeras containing only the alpha3 and cytoplasmic domains could upregulate hepcidin expression. Since the HFE alpha3 domain interacts with TfR2, these results supported our finding that TfR2/HFE complex is required for transcriptional regulation of hepcidin by holo-Tf.
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Registered trials
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