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In an ischemic stroke model, exendin-4 enhanced the activation of PI3K/Akt/CREB signaling, leading to upregulation of APE1, a key enzyme responsible for resolving oxidized bases and single-strand breaks, which reduced nuclear DNA fragmentation and preserved neuronal viability (75, 76)

doi:10.1038/s41467-024-50199-y 215

PMCID: PMC13218929
