Activation of JNK pathway in persistent pain.
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.
Gao
Yong-Jing
YJ
Pain Research Center, Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Ji
Ru-Rong
RR
D000818:Animals; D004789:Enzyme Activation; D006801:Humans; D048670:MAP Kinase Kinase 4 / Q000378:metabolism*; D010146:Pain / Q000201:enzymology*; D015398:Signal Transduction / Q000502:physiology*
D048670:MAP Kinase Kinase 4