Glial Contributions to Neuropathic Pain: Central and Peripheral Strategies in Postherpetic Neuralgia Pathogenesis and Therapeutics

Neuropathic pain (NP), particularly postherpetic neuralgia (PHN), involves intricate mechanisms that extend far beyond neuronal dysfunction. In recent years, glial cell-mediated neuro-immune-inflammatory circuits mediated by glial cells (including spinal microglia, astrocytes, and dorsal root ganglion satellite glia) have been regarded as one of the key pathological mechanisms for the occurrence and maintenance of NP. Glial cells exacerbate pain pathogenesis by driving neuroinflammation, amplifying nociceptive signaling, and modulating ion channels and pain-related signaling molecules. A systematic review of glial molecular and network alterations, correlated with the typical clinical phenotype of PHN, may provide practical clues for precise stratified therapy, drug repositioning, and novel targeted interventions (such as glial modulators, neuronutrition support, and neuro-immune pathway modulation). This review aims to summarize the latest progress in glial cells and neuropathic pain, with a focus on discussing its implications and suggestions for the treatment strategies of PHN.