ALKBH5 Modulates Asthma Progression by Downregulating N6-methyladenosine Methylation

Knockdown of ALKBH5 significantly elevated the survival and colony formation ability of bronchial epithelial cells in an IL-13 induction model.

• Depletion of ALKBH5 is associated with increased levels of total iron, Fe2+, lipid reactive oxygen species (ROS), and malondialdehyde (MDA) in bronchial epithelial cells.
• A reduction in superoxide dismutase (SOD) levels was observed in IL-13-induced bronchial epithelial cells following ALKBH5 knockdown.
• Increased enrichment of N6-methyladenosine methylation (m6A) and expression of glutathione peroxidase 4 (GPX4) was noted with ALKBH5 depletion.
• Inhibition of GPX4 reversed the pro-proliferation and anti-ferroptosis effects resulting from ALKBH5 knockdown.
• The findings suggest that ALKBH5 plays a regulatory role in the proliferation of bronchial epithelial cells and their response to ferroptosis.

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