Investigations by Sangokoya et al provide evidence that elevated miR-144 in HbSS erythroid cells from SCD patients with severe anemia can compromise antioxidizing capacities.2 Mechanistically, this may involve miR-144 decay of transcripts for NRF2, a CNC-bZip transcription factor known to regulate several antioxidant genes (A). Panel B outlines (in black font) roles for miR-144/451 as discovered this year via novel knockout mouse models. For erythroid HbSS cells (blue font), interesting parallel questions concerning mechanisms of miR-144/451 dysregulation are raised within a SCD context.
