Int. J. Mol. Sci., 2022 · DOI: https://doi.org/10.3390/ijms23052685 · Published: February 28, 2022
Neuropathic pain, resulting from damage to the somatosensory system, poses significant management and treatment challenges, highlighting the urgent need for novel therapeutic strategies. Autophagy and apoptosis, crucial adaptive mechanisms in neurons under stress or damage, exhibit altered activities post-nerve damage, influencing myelin clearance, nerve regeneration, and pain behavior. The interplay between autophagy, apoptosis, and pro-inflammatory cytokines in the nervous system offers potential therapeutic targets for neuropathic pain by modulating apoptotic/autophagic activities and proinflammatory cytokine levels.
Agents enhancing autophagy and suppressing apoptosis in injured nerves and dorsal root ganglia hold promise for neuropathic pain treatment.
Modulating autophagy, apoptosis, and pro-inflammatory cytokines presents a potential therapeutic strategy for neuropathic pain.
Further research is needed to elucidate the detailed mechanisms of autophagy, apoptosis, and their interactions with pro-inflammatory cytokines in neuropathic pain formation in the spinal cord.