ArticleiScience2026
Pathological frataxin deficiency in mice causes tissue-specific alterations in iron homeostasis.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Visual Pathways Involvement in Friedreich's Ataxia Patients Without Macular Impairment.Journal of clinical medicine · 2026Article
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Authors and funding
11 authors.
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Abstract
Friedreich ataxia is caused by partial frataxin deficiency due to genetic mutations. It is well established that frataxin knockout affects iron homeostasis, but the alterations caused by pathological (partial) frataxin deficiency are poorly understood. In this study, we have analyzed iron homeostasis in a mouse model presenting pathological frataxin deficiency (FXNI151F). Our results reveal tissue-specific alterations of iron regulatory proteins (IRPs). In the heart, IRP2 accumulation is observed, likely triggered by iron-sulfur deficiency, while IRP1 is decreased in the cerebellum and liver. We also found elevated iron levels in mutant mice. Accumulation was particularly pronounced in the cerebellum, where increases were already evident at 10 weeks. Hepatic accumulation was not manifested until 21 weeks and was more pronounced in females. Overall, these findings indicate that frataxin deficiency disrupts iron homeostasis in a tissue-, age-, and sex-dependent manner, and provide novel insights into the mechanisms causing these perturbations.
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