Activation of JNK pathway in persistent pain.

Journal Article (Journal Article;Review)

The c-Jun N-terminal kinase (JNK) is a stress-activated member of MAP kinase family. JNK activation has been strongly implicated in inflammatory responses, neurodegeneration, and apoptosis. Recent evidence shows that JNK pathway is also transiently activated in primary sensory neurons after tissue or nerve injury, which is required for the development of hyperalgesia and allodynia. In particular, JNK is persistently activated in astrocytes of the spinal cord after nerve injury, and this activation can maintain central sensitization and mechanical allodynia. In this mini-review, we will provide evidence for the involvement of JNK pathway in regulating persistent pain sensitization. We will also discuss possible upstream signaling mechanisms that cause JNK activation and downstream signaling mechanisms by which JNK modulates pain sensitivity. Thus, targeting JNK pathway might be a useful strategy to treat both neurodegeneration and chronic pain.

Full Text

Duke Authors

Cited Authors

  • Gao, Y-J; Ji, R-R

Published Date

  • June 6, 2008

Published In

Volume / Issue

  • 437 / 3

Start / End Page

  • 180 - 183

PubMed ID

  • 18455869

Pubmed Central ID

  • PMC2486445

International Standard Serial Number (ISSN)

  • 0304-3940

Digital Object Identifier (DOI)

  • 10.1016/j.neulet.2008.03.017


  • eng

Conference Location

  • Ireland