Reactivating the silenced embryonic ζ-globin gene restores therapeutic hemoglobin levels in severe α-thalassemia models, including lethal forms like Hb Bart's hydrops fetalis.
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Hemoglobinopathies and Related Disorders
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The CYB5R3 T117S variant reduces riociguat efficacy by impairing nitric oxide signaling in sickle cell disease patients.
- Open access
Elevated blood-brain barrier permeability in sickle cell disease correlates with microstructural brain injury, with 79 plasma proteins linked to systemic pathways influencing BBB disruption.
Exa-cel therapy achieved transfusion independence or absence of severe vaso-occlusive crises in children aged 5 to 11 with transfusion-dependent β-thalassemia or sickle cell disease, respectively, over 16 months.
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Long-term BCL11A silencing via shmiR vector in Sickle Cell Disease shows durable HbF induction and sustained clinical benefits over 48 months.
Selective disruption of EZH2 exon 14 in PRC2 reactivates fetal hemoglobin in adult erythroid cells while preserving cell fitness.
Haploidentical stem cell transplantation is consistently more cost-effective than gene therapy for sickle cell disease, with a 100% probability across analyses.
RAAS inhibitors significantly decrease hemoglobin levels in sickle cell disease patients and mouse models, worsening anemia by approximately 0.5 g/dL.
- Open access
Loss of Stag2 causes GATA1 to reprogram its binding from erythroid to megakaryocyte targets, disrupting normal blood cell development in MDS models.
- Open access
Polygenic risk scores and family history together improve coronary heart disease prediction across diverse US populations, increasing true-positive detection by nearly 19%.
Mitochondrial haem scarcity is detected by an ancient OMA1-DELE1 pathway that regulates translation during erythroid development, conserved across species including invertebrates.
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