METTL14 promotes ischemic stroke pathogenesis by mediating m6A methylation modification of BACH1 to enhance OGD/R-induced neuronal damage and facilitate ferroptosis in SK-N-SH cells | Synapse
March 3, 2026
METTL14 promotes ischemic stroke pathogenesis by mediating m6A methylation modification of BACH1 to enhance OGD/R-induced neuronal damage and facilitate ferroptosis in SK-N-SH cells
Key Points
METTL14 mediates m6A methylation, promoting neuronal damage and ferroptosis in cells.
Neuronal damage was significantly increased with METTL14 activity, showing a 30% rise in injury markers.
Assessment of SK-N-SH cells during OGD/R identified key pathways involving BACH1 and m6A methylation.
These findings highlight the potential for developing therapies targeting METTL14 to reduce ischemic stroke damage.