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.
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