Activation of JNK pathway in persistent pain

NEUROSCIENCE LETTERS

卷:437

Article

Gao, Yong-Jing¹  Ji, Ru-Rong¹ 

[1] Harvard Univ, Sch Med, Dept Anesthesiol, Brigham & Womens Hosp,Pain Res Ctr, Boston, MA 02115 USA

关键词: MAP kinase;    chronic pain;    neuropathic pain;    dorsal root ganglion;    spinal cord;    signal transduction;   

DOI  :  10.1016/j.neulet.2008.03.017

来源: Elsevier

【 摘 要 】

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. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

【 授权许可】

Free