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神经炎症驱动的慢性疼痛中的新兴靶点。

Emerging targets in neuroinflammation-driven chronic pain.

作者信息

Ji Ru-Rong, Xu Zhen-Zhong, Gao Yong-Jing

机构信息

Departments of Anesthesiology and Neurobiology, Duke University Medical Center, 595 LaSalle Street, Durham, North Carolina 27710, USA.

Pain Research Laboratory, Institute of Nautical Medicine, Jiangsu Key laboratory of Neuroregeneration, Nantong University, 19 Qixiu Road, Nantong 226001, Jiangsu 226001, China.

出版信息

Nat Rev Drug Discov. 2014 Jul;13(7):533-48. doi: 10.1038/nrd4334. Epub 2014 Jun 20.

Abstract

Current analgesics predominately modulate pain transduction and transmission in neurons and have limited success in controlling disease progression. Accumulating evidence suggests that neuroinflammation, which is characterized by infiltration of immune cells, activation of glial cells and production of inflammatory mediators in the peripheral and central nervous system, has an important role in the induction and maintenance of chronic pain. This Review focuses on emerging targets - such as chemokines, proteases and the WNT pathway - that promote spinal cord neuroinflammation and chronic pain. It also highlights the anti-inflammatory and pro-resolution lipid mediators that act on immune cells, glial cells and neurons to resolve neuroinflammation, synaptic plasticity and pain. Targeting excessive neuroinflammation could offer new therapeutic opportunities for chronic pain and related neurological and psychiatric disorders.

摘要

目前的镇痛药主要调节神经元中的疼痛转导和传递,在控制疾病进展方面成效有限。越来越多的证据表明,神经炎症在外周和中枢神经系统中以免疫细胞浸润、胶质细胞激活以及炎症介质产生为特征,在慢性疼痛的诱导和维持中起重要作用。本综述聚焦于促进脊髓神经炎症和慢性疼痛的新兴靶点,如趋化因子、蛋白酶和WNT信号通路。它还强调了抗炎和促消退脂质介质,这些介质作用于免疫细胞、胶质细胞和神经元以消退神经炎症、恢复突触可塑性并缓解疼痛。针对过度的神经炎症可能为慢性疼痛以及相关的神经和精神疾病提供新的治疗机会。

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