In this issue of Blood, Makarona et al demonstrate that histone deacetylase (HDAC) inhibitors (HDACis) in glucose-6-phosphate dehydrogenase (G6PD)-deficient cells reinstates enzyme activity by boosting gene transcription. This therapeutic approach opens new avenues for preclinical and clinical studies to treat not only chronic nonspherocytic hemolytic anemia caused by severe G6PD variants, but also other genetic diseases.
Keyphrases
- histone deacetylase
- copy number
- genome wide
- induced apoptosis
- dna methylation
- cell cycle arrest
- chronic kidney disease
- gene expression
- cell therapy
- transcription factor
- drug induced
- blood glucose
- stem cells
- type diabetes
- weight loss
- cell proliferation
- mesenchymal stem cells
- insulin resistance
- bone marrow
- skeletal muscle