Iron-Dependent Liver Fibrogenesis in Mice
Author Information
Author(s): Sebastiani Giada, Gkouvatsos Kostas, Maffettone Carmen, Busatto Graziella, Guido Maria, Pantopoulos Kostas
Primary Institution: Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, Quebec, Canada
Hypothesis
Hepatic iron overload exacerbates liver damage and fibrogenesis in Hjv-/- mice treated with CCl4.
Conclusion
Hjv-/- mice show accelerated liver damage and fibrosis due to iron overload when treated with CCl4.
Supporting Evidence
- Hjv-/- mice developed earlier and more severe liver damage compared to wild type mice.
- Serum ferritin levels increased dramatically in Hjv-/- mice after CCl4 treatment.
- Hepatic iron overload was confirmed by histological analysis.
- Profibrogenic gene expression was significantly higher in Hjv-/- mice.
- Oxidative stress markers were elevated in Hjv-/- mice even without CCl4 treatment.
Takeaway
Mice with a genetic condition that causes iron overload get hurt faster and worse when given a liver toxin compared to normal mice.
Methodology
Hjv-/- and wild type mice were treated with CCl4 to induce liver injury, and various biochemical and histological analyses were performed.
Potential Biases
Potential bias in interpretation due to the use of a single animal model.
Limitations
The study primarily focuses on a specific mouse model, which may not fully replicate human conditions.
Participant Demographics
Hjv-/- mice and wild type controls, both maintained on an inbred background.
Statistical Information
P-Value
p<0.0001
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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