Advances of the PI3K/AKT/mTOR Pathway in the Neural Repair of Spinal Cord Injury

Abstract

Spinal cord injury (SCI) induces catastrophic neurological deficits, activating multiple signaling pathways, notably the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) pathway. Current treatments primarily offer symptomatic relief without addressing underlying pathophysiology. Emerging research highlights the PI3K/AKT/mTOR pathway’s crucial role in regulating neuronal survival, axon regeneration, glial responses, autophagy, and immune modulation post-SCI. Modulating this pathway post-injury shows promise in reducing inflammation, apoptosis, and neuropathic pain, while promoting neural repair. Given its central role, the PI3K/AKT/mTOR pathway is identified as a key therapeutic target for SCI management. This review summarizes current knowledge on SCI pathology, details the PI3K/AKT/mTOR pathway’s characteristics, and explores its dual roles in pathology and therapeutic interventions, aiming to provide a comprehensive reference for future SCI research and targeted therapies.