期刊
NEUROSCIENCE LETTERS
卷 437, 期 3, 页码 180-183出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2008.03.017
关键词
MAP kinase; chronic pain; neuropathic pain; dorsal root ganglion; spinal cord; signal transduction
资金
- FIC NIH HHS [R03 TW007180-03, TW7180, R03 TW007180] Funding Source: Medline
- NIDCR NIH HHS [DE17794, R01 DE017794, R01 DE017794-02, R01 DE017794-03] Funding Source: Medline
- NINDS NIH HHS [R01 NS054932-02, NS 54932, R01 NS054932, R01 NS054932-01A1] Funding Source: Medline
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据