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Long-term PAEC loss will selectively preserve PAECs that are tolerant to apoptosis and overproliferate, eventually leading to irreversible intimal hyperplasia and plexiform lesions [24, 26]

In STZ-induced DKD mice, it has been observed that PI3K/AKT activity is significantly elevated, whereas AMPK activity is markedly reduced, thereby promoting apoptosis (213, 214)