| Summary: | Hemoglobin F (HbF, α2γ2) is a major contributor to the clinical heterogeneity and ameliorating agent observed in patients with the β-globin disorders including β-thalassemia and sickle cell disease (SCD). During fetal life, HbF is the major hemoglobin but is largely substituted by adult hemoglobin (HbA, α2β2) following a globin expression switch after birth. Increased γ-globin expression can reduce the clinical severity of β-thalassemia and SCD. Therefore, increase in HbF production has served as a longstanding goal. The progression of target-based therapeutics has been confused by limited comprehension of molecular mechanisms of gamma-globin gene expression. However, recent discoveries of regulators of HbF level represent a major development and provide new opportunities in employing novel rational therapeutic strategies. In this review, molecular mechanisms of hemoglobin F induction will be discussed.
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