漏钠离子通道参与神经病理性疼痛机制的研究进展
Research advances of sodium leak channel contributes to neuropathic pain
王旭燕 1魏义勇 1王海英1
作者信息
- 1. 遵义医科大学附属医院麻醉科,遵义 563000
- 折叠
摘要
神经病理性疼痛(NP)是临床上常见的一种慢性疼痛,发病率高,治疗难度大,严重影响患者的生活质量,其发病机制和治疗靶点一直是医学研究的热点和难点.漏钠离子通道(NALCN)是一种与电压无关、非选择性、非失活的阳离子通道,在NP的发生过程中扮演重要角色.文章就NALCN的结构和功能,NALCN通过中枢敏化、外周敏化、调节P物质(SP)的致痛效应以及环腺苷酸(cAMP)/蛋白激酶A(PKA)信号通路参与NP的有关机制进行综述,以期为NP发生机制的研究和治疗提供新方向.
Abstract
Neuropathic pain(NP)is a common chronic pain in clinical practice,with a character of high incidence and refrac-tory to treatment,which seriously affects the quality of patients'life.Its pathogenesis and therapeutic targets have always been the fo-cus and difficulty of medical research.Sodium leak channel non-selective protein(NALCN)is a kind of voltage-independent,non-selective,and non-inactivating cation channel,which plays an important role in the generation of NP.The review summarizes re-cent study achievements on the structure and function of NALCN and variations mechanism to the NALCN involving in NP,including central sensitization,peripheral sensitization,regulation of the pain-inducing effects of substance P(SP),and cyclic adenylic acid(cAMP)/protein kinase A(PKA)signaling pathway,in order to provide a new direction for neuropathic pain study and treatment.
关键词
神经病理性疼痛/漏钠离子通道/中枢敏化/外周敏化/P物质/环腺苷酸/蛋白激酶AKey words
Neuropathic pain/Sodium leak channel non-selective protein/Central sensitization/Peripheral sensitiza-tion/Substance P/Cyclic adenylic acid/Protein kinase A引用本文复制引用
出版年
2024
NETL
NSTL
万方数据