ArticleBlood advances2024
Mitoxantrone ameliorates ineffective erythropoiesis in a β-thalassemia intermedia mouse model.
Article in Blood advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Fertility and endocrinopathies among adults with β-thalassemia major treated at Dubai thalassemia center.Frontiers in endocrinology · 2026Observational
- Are Mitochondria a Potential Target for Treating β-Thalassemia?Journal of clinical medicine · 2025Review
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Authors and funding
11 authors.
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Abstract
abstractβ-thalassemia is a condition characterized by reduced or absent synthesis of β-globin resulting from genetic mutations, leading to expanded and ineffective erythropoiesis. Mitoxantrone has been widely used clinically as an antitumor agent considering its ability to inhibit cell proliferation. However, its therapeutic effect on expanded and ineffective erythropoiesis in β-thalassemia is untested. We found that mitoxantrone decreased α-globin precipitates and ameliorated anemia, splenomegaly, and ineffective erythropoiesis in the HbbTh3/+ mouse model of β-thalassemia intermedia. The partially reversed ineffective erythropoiesis is a consequence of effects on autophagy as mitochondrial retention and protein levels of mTOR, P62, and LC3 in reticulocytes decreased in mitoxantrone-treated HbbTh3/+ mice. These data provide significant preclinical evidence for targeting autophagy as a novel therapeutic approach for β-thalassemia.
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