Fig. 8.

Comparison of prokineticin system alterations in inflammatory and neuropathic pain. In inflammatory and neuropathic pain, the production of circulating factors shifts toward those with a pro- inflammatory phenotype. PK2 is highly upregulated and blocking its receptors inhibits hyperalgesia in both inflammatory and neuropathic pain. Interestingly, the largest gap in our knowledge is the role of PK2 splicing variants in neuropathic pain and the involvement of the PKR2 pathway in inflammatory pain. Created with BioRender.com.