ArticleCells2026
CCND3 Suppression Ameliorates β-Thalassaemia in a Murine Disease Model: A Potential Therapeutic Strategy.
Article in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
β-thalassaemia (β-thal) is part of a group of diseases, the β-hemoglobinopathies, affecting the levels or functionality of the β-globin subunit of hemoglobin, which are the most widespread monogenic diseases throughout the world. The severity of β-thal is determined by different genetic factors, but in the gravest form, affected patients are constrained to a program of blood transfusion and iron chelation regimens for their entire life. Although definitive cures, such as bone marrow transplantation or gene therapy, are now available, they are still far from being applied worldwide. Therefore, there is growing attention towards the use of drugs to cure or ameliorate β-thal disorder. Among all the strategies, pharmacological increase of fetal HbF and/or adult HbA2 can represent an advantageous approach as high levels of both hemoglobins are effective against β-thal. Therefore, the identification of therapeutic targets that can modulate, by the use of drugs, these hemoglobins is increasingly urgent. In this paper, we analyze the effects of the absence of the
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