Activation of JNK pathway in persistent pain
Activation of JNK pathway in persistent pain
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DOI：
10.1016/j.neulet.2008.03.017
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发表时间：
2008-06-06
影响因子：
2.5
通讯作者：
Ji, Ru-Rong
中科院分区：
文献类型：
--
作者：
Gao, Yong-Jing;Ji, Ru-Rong
C-Jun氨基末端激酶(JNK)是MAP激酶家族中一个应激激活的成员。JNK的激活与炎症反应、神经变性和细胞凋亡密切相关。最近的证据表明，在组织或神经损伤后，初级感觉神经元中的JNK通路也被一过性地激活，这是痛觉过敏和痛觉过敏发生所必需的。特别是，JNK在神经损伤后脊髓星形胶质细胞中持续激活，这种激活可以维持中枢敏化和机械性痛觉异常。在这篇简短的综述中，我们将提供JNK通路参与调节持续性疼痛敏化的证据。我们还将讨论引起JNK激活的可能的上游信号机制和JNK调节疼痛敏感性的下游信号机制。因此，靶向JNK通路可能是治疗神经变性和慢性疼痛的有效策略。(C)2008爱思唯尔爱尔兰有限公司。保留所有权利。
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.