ArticleBMC systems biology2017
Modeling the dynamics of mouse iron body distribution: hepcidin is necessary but not sufficient.
Article in BMC systems biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Mathematical modeling reveals ferritin as the strongest cellular driver of dietary iron transfer block in enterocytes.PLoS computational biology · 2025Article
- Computational Prediction of Tissue Iron Dynamics in Iron Deficiency Anemia Following Intravenous Ferric Carboxymaltose Therapy.International journal of nanomedicine · 2025Article
- BioModels Parameters: a treasure trove of parameter values from published systems biology models.Bioinformatics (Oxford, England) · 2020Article
- Association of serum ferritin with metabolic syndrome in eight cities in China.Food science & nutrition · 2020Article
- Animal Models of Normal and Disturbed Iron and Copper Metabolism.The Journal of nutrition · 2019Review
- Gastrointestinal iron excretion and reversal of iron excess in a mouse model of inherited iron excess.Haematologica · 2019Article
- Oral Gavage of Ginger Nanoparticle-Derived Lipid Vectors Carrying Dmt1 siRNA Blunts Iron Loading in Murine Hereditary Hemochromatosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- A computational model to understand mouse iron physiology and disease.PLoS computational biology · 2019Article
- No effects without causes: the Iron Dysregulation and Dormant Microbes hypothesis for chronic, inflammatory diseases.Biological reviews of the Cambridge Philosophical Society · 2018Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundIron is an essential element of most living organisms but is a dangerous substance when poorly liganded in solution. The hormone hepcidin regulates the export of iron from tissues to the plasma contributing to iron homeostasis and also restricting its availability to infectious agents. Disruption of iron regulation in mammals leads to disorders such as anemia and hemochromatosis, and contributes to the etiology of several other diseases such as cancer and neurodegenerative diseases. Here we test the hypothesis that hepcidin alone is able to regulate iron distribution in different dietary regimes in the mouse using a computational model of iron distribution calibrated with radioiron tracer data.
resultsA model was developed and calibrated to the data from adequate iron diet, which was able to simulate the iron distribution under a low iron diet. However simulation of high iron diet shows considerable deviations from the experimental data. Namely the model predicts more iron in red blood cells and less iron in the liver than what was observed in experiments.
conclusionsThese results suggest that hepcidin alone is not sufficient to regulate iron homeostasis in high iron conditions and that other factors are important. The model was able to simulate anemia when hepcidin was increased but was unable to simulate hemochromatosis when hepcidin was suppressed, suggesting that in high iron conditions additional regulatory interactions are important.
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