ArticleAntioxidants & redox signaling2015
HJV and HFE Play Distinct Roles in Regulating Hepcidin.
Article in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Pooled it
- Article
- New Deferric Amine Compounds Efficiently Chelate Excess Iron to Treat Iron Overload Disorders and to Prevent Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Evidence That HFE H63D Variant Is a Potential Disease Modifier in Cluster Headache.Journal of molecular neuroscience : MN · 2022Article
- Repurposing ICG enables MR/PA imaging signal amplification and iron depletion for iron-overload disorders.Science advances · 2021Article
- HFE inhibits type I IFNs signaling by targeting the SQSTM1-mediated MAVS autophagic degradation.Autophagy · 2021Article
- Hepcidin Signaling in Health and Disease: Ironing Out the Details.Hepatology communications · 2021Review
- Hemojuvelin is a novel suppressor for Duchenne muscular dystrophy and age-related muscle wasting.Journal of cachexia, sarcopenia and muscle · 2019Article
- Liver iron sensing and body iron homeostasis.Blood · 2019Review
- Minor variant of rs 16827043 in the iron regulator hemojuvelin gene (HJV) contributes to hypertension: The TAMRISK study.Medicine · 2017Article
- Hemojuvelin regulates the innate immune response to peritoneal bacterial infection in mice.Cell discovery · 2017Article
- Blood and iron.Journal of molecular medicine (Berlin, Germany) · 2015Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsHereditary hemochromatosis (HH) is an iron overload disease that is caused by mutations in HFE, HJV, and several other genes. However, whether HFE-HH and HJV-HH share a common pathway via hepcidin regulation is currently unclear. Recently, some HH patients have been reported to carry concurrent mutations in both the HFE and HJV genes. To dissect the roles and molecular mechanisms of HFE and/or HJV in the pathogenesis of HH, we studied Hfe(-/-), Hjv(-/-), and Hfe(-/-)Hjv(-/-) double-knockout mouse models.
resultsHfe(-/-)Hjv(-/-) mice developed iron overload in multiple organs at levels comparable to Hjv(-/-) mice. After an acute delivery of iron, the expression of hepcidin (i.e., Hamp1 mRNA) was increased in the livers of wild-type and Hfe(-/-) mice, but not in either Hjv(-/-) or Hfe(-/-)Hjv(-/-) mice. Furthermore, iron-induced phosphorylation of Smad1/5/8 was not detected in the livers of Hjv(-/-) or Hfe(-/-)Hjv(-/-) mice. INNOVATION: We generated and phenotypically characterized Hfe(-/-)Hjv(-/-) double-knockout mice. In addition, because they faithfully phenocopy clinical HH patients, these mouse models are an invaluable tool for mechanistically dissecting how HFE and HJV regulate hepcidin expression.
conclusionsBased on our results, we conclude that HFE may depend on HJV for transferrin-dependent hepcidin regulation. The presence of residual hepcidin in the absence of HFE suggests either the presence of an unknown regulator (e.g., TFR2) that is synergistic with HJV or that HJV is sufficient to maintain basal levels of hepcidin.
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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.