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Ectopic discharges, sympathetic effects, transcription dysregulation of pain-related genes, conduction changes in pain signaling, aberrant activation of neuroglial cells, and alterations in the function of the central nervous system (CNS) after nerve injury are all potential contributors to develop peripheral and central sensitization [26, 31] (Table 2)

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microRNA-592 blockade inhibits oxidative stress injury in Alzheimer’s disease astrocytes via the KIAA0319-mediated Keap1/Nrf2/ARE signaling pathway