Hello All!
Fetal hemoglobin (HbF) is the primary oxygen transport protein in the human fetus. Its ability to more efficiently bind oxygen is crucial to the early stages of development. It continues to perform this role in the newborn until the sixth postnatal month, by which time is it almost completely replaced by adult hemoglobin. Certain blood disorders result in the continued production of HbF and in adults, its production can be pharmacologically reactivated.
HbF has been found to mitigate the effects of vaso-occlusive crises in SCD patients. This is likely as a result of its high oxygen affinity. This makes it useful to the management and treatment of SCD, especially in the prevention of vaso-occlusive crises which are triggered by low oxygenation. Research into the genes involved in HbF expression and silencing are hence key factor in the fight against SCD. In a study carried out in Northern Brazil, Cardoso et al. recently identified the alleles which primarily influence the production of high levels of HbF. Suzuki et al, also released a paper which explores the molecular mechanisms which control fetal globin gene silencing. Furthermore, according to a Science Daily report, researchers at Kings College, London have also successfully traced the global distribution of beneficial variants of genes involved in red blood cell development and HbF production in adults. These revelations have important implications for future therapies targetting SCD and other hemoglobinopathies.
In other SCD related developments:
Have a great weekend!
The ASN Team
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