The function of chemokine-driven glial-neuronal interaction in chronic pain
Jie Zheng
Chronic pain affects hundreds of millions worldwide, yet current treatments—from NSAIDs to opioids—fall short and bring unwanted side effects. Neuroinflammation drives bidirectional glial-neuronal communication, a core mechanism underlying central sensitization in chronic pain, with chemokines serving as key mediators. Most studies to date have zeroed in on isolated pathways or specific anatomical sites, missing the bigger picture. We pull together findings across the neural axis, spanning perip