Gao Yong-Jing, Ji Ru-Rong
Pain Research Center, Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Neurosci Lett. 2008 Jun 6;437(3):180-3. doi: 10.1016/j.neulet.2008.03.017. Epub 2008 Mar 13.
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-Jun氨基末端激酶（JNK）是丝裂原活化蛋白激酶（MAPK）家族的应激激活成员。JNK的激活与炎症反应、神经退行性变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通路也会短暂激活，这是痛觉过敏和异常性疼痛发展所必需的。特别是，神经损伤后脊髓星形胶质细胞中的JNK持续激活，这种激活可维持中枢敏化和机械性异常性疼痛。在本综述中，我们将提供证据证明JNK通路参与调节持续性疼痛敏化。我们还将讨论导致JNK激活的可能上游信号机制以及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退行性变和慢性疼痛的有效策略。
