Figure 1.

The mechanisms of Janus Kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) in chronic pain. After extracellular signal/stimulation, the JAK2/STAT3 signaling pathway is activated by several proinflammatory cytokines and GM-CSF that are released by activated microglia and astrocytes. On the one hand, JAK2/STAT3 affects the translation and expression of IL-6, IL-1β, TNF-α, IL-33, CCL2 and SOCS3 to trigger neuroinflammatory chronic ain. On the other hand, JAK2/STAT3 promotes the NMDAR pathway to induce peripheral sensitization and chronic pain. However, IL-10, TGF-β, and α7nAchR can inhibit these mechanisms.