METTL16 Promotes Cerebral Ischemia-Reperfusion Injury via m6A-Dependent Upregulation of TIPARP

Background: A) methyltransferase METTL16 has emerged as a key regulator of RNA metabolism, but its specific role and mechanism in ischemic stroke remain unclear. Methods: A-RIP-qPCR. Protein stability was determined using cycloheximide chase assay. Rescue experiments were performed by overexpressing TIPARP in METTL16-depleted cells. Results: A modification, thereby stabilizing TIPARP transcripts and upregulating TIPARP protein expression. Critically, TIPARP overexpression completely abolished the protective effects of METTL16 knockdown against OGD-induced apoptosis and synaptic impairment. Conclusion: A-TIPARP axis represents a novel pathogenic mechanism and a potential therapeutic target for ischemic stroke.