ArticleThe Journal of clinical investigation2010
Hepcidin mediates transcriptional changes that modulate acute cytokine-induced inflammatory responses in mice.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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Who cites it
86 citing papers in PubMed, 202 citations in OpenAlex.
- The effect of iron loading and iron chelation on the innate immune response and subclinical organ injury during human endotoxemia: a randomized trial.Haematologica · 2014Trial
- Intra-graft expression of genes involved in iron homeostasis predicts the development of operational tolerance in human liver transplantation.The Journal of clinical investigation · 2012Trial
- Animal models of anemia of inflammation: Methodological advances, limitations, and translational applications.Animal models and experimental medicine · 2026Review
- The diagnostic accuracy of serum and synovial inflammatory markers in chronic periprosthetic joint infection among anaemic patients.Bone & joint research · 2026Article
- Protective Effect of Hepcidin on Sepsis-Associated Acute Kidney Injury via Activating the Nrf2/GPX4 Signaling Pathway.Current issues in molecular biology · 2025Article
- Serum Hepcidin Levels in Breast Cancer Patients: Investigating the Correlation to Tumor Stage-A Cross-Sectional Study.Health science reports · 2025Article
- Targeting hepcidin in colorectal cancer triggers a TNF-dependent-gasdermin E-driven immunogenic cell death response.Experimental hematology & oncology · 2024Article
- The Iron Metabolism with a Specific Focus on the Functioning of the Nervous System.Biomedicines · 2024Review
- Hepcidin deficiency impairs hippocampal neurogenesis and mediates brain atrophy and memory decline in mice.Journal of neuroinflammation · 2024Article
- Nervous Necrosis Virus Modulation of European Sea Bass (International journal of molecular sciences · 2023Article
- Monocyte MRI Relaxation Rates Are Regulated by Extracellular Iron and Hepcidin.International journal of molecular sciences · 2023Article
- Understanding How Minerals Contribute to Optimal Immune Function.Journal of immunology research · 2023Review
- Article
- Active Compounds in Fruits and Inflammation in the Body.Nutrients · 2022Review
- Iron-accumulating splenocytes may exacerbate non-alcoholic steatohepatitis through the production of proinflammatory cytokines and reactive oxygen species.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Circulating hepcidin and its associations with low-grade inflammation and iron indices among Arab adults with and without T2DM.American journal of translational research · 2022Article
- Article
- Immunomodulatory streptococci that inhibit CXCL8 secretion and NFκB activation are common members of the oral microbiota.Journal of medical microbiology · 2021Article
- Stressed erythrophagocytosis induces immunosuppression during sepsis through heme-mediated STAT1 dysregulation.The Journal of clinical investigation · 2021Article
- Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Hepcidin is a peptide hormone that regulates iron homeostasis and acts as an antimicrobial peptide. It is expressed and secreted by a variety of cell types in response to iron loading and inflammation. Hepcidin mediates iron homeostasis by binding to the iron exporter ferroportin, inducing its internalization and degradation via activation of the protein kinase Jak2 and the subsequent phosphorylation of ferroportin. Here we have shown that hepcidin-activated Jak2 also phosphorylates the transcription factor Stat3, resulting in a transcriptional response. Hepcidin treatment of ferroportin-expressing mouse macrophages showed changes in mRNA expression levels of a wide variety of genes. The changes in transcript levels for half of these genes were a direct effect of hepcidin, as shown by cycloheximide insensitivity, and dependent on the presence of Stat3. Hepcidin-mediated transcriptional changes modulated LPS-induced transcription in both cultured macrophages and in vivo mouse models, as demonstrated by suppression of IL-6 and TNF-alpha transcript and secreted protein. Hepcidin-mediated transcription in mice also suppressed toxicity and morbidity due to single doses of LPS, poly(I:C), and turpentine, which is used to model chronic inflammatory disease. Most notably, we demonstrated that hepcidin pretreatment protected mice from a lethal dose of LPS and that hepcidin-knockout mice could be rescued from LPS toxicity by injection of hepcidin. The results of our study suggest a new function for hepcidin in modulating acute inflammatory responses.
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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.