Elevated CDKN1A (P21) mediates β-thalassemia erythroid apoptosis, but its loss does not improve β-thalassemic erythropoiesis
Liang R, Lin M, Menon V, Qiu J, Menon A, Breda L, Arif T, Rivella S, Ghaffari S. Elevated CDKN1A (P21) mediates β-thalassemia erythroid apoptosis, but its loss does not improve β-thalassemic erythropoiesis. Blood Advances 2023, 7: 6873-6885. PMID: 37672319, PMCID: PMC10685172, DOI: 10.1182/bloodadvances.2022007655.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisBeta-ThalassemiaCyclin-Dependent Kinase Inhibitor p21ErythropoiesisHumansSplenomegalyConceptsErythroid cell maturationErythroid cell survivalCell cycle inhibitor Cdkn1aFoxO3 target genesErythroid apoptosisFoxO3 transcription factorElevated reactive oxygen speciesΒ-globin geneCell maturationEmbryonic lethalityTranscription factorsTarget genesErythroid maturationReactive oxygen speciesMolecular networksMolecular mechanismsThalassemic erythropoiesisCell survivalProgenitor compartmentErythroid compartmentFOXO3Extramedullary erythropoiesisΒ-thalassemiaApoptosisHemoglobin production