《生命科学》 2025, 37(6): 663-671
钾-氯协同转运蛋白2在神经病理性疼痛中的研究进展
摘 要:
神经病理性疼痛(neuropathic pain, NP) 发病率高,机制复杂,现有的治疗方案疗效不佳,严重影响患者的生活质量。越来越多的研究表明钾- 氯协同转运蛋白2 (K+-Cl− cotransporter, KCC2) 通过将细胞内钾离子和氯离子一起转运到细胞外,维持胞内低氯水平,是超极化抑制信号传导的核心。KCC2 表达下调或KCC2 的活性降低,导致胞内氯离子浓度增加,神经元去极化,神经系统兴奋性升高,引起NP。探究KCC2 的作用机制有助于了解NP 发病、预防和治疗。本文将从KCC2 的结构和功能,及其参与调控NP的相关机制展开讨论,旨在为NP 的预防和治疗提供新思路。
通讯作者:思永玉 , Email:siyongyu@kmmu.edu.cn
Abstract:
The incidence of neuropathic pain is high, and the pathogenesis is complex, and the current treatment regimens are not effective, which seriously affects the quality of life of patients. A growing number of studies have shown that K+-Cl-cotransporter 2 (KCC2) maintains intracellular low chlorine levels by transporting intracellular potassium and chloride ions together to the outside of the cell, which is the core of hyperpolarization inhibition of signal transduction. A decrease in the expression or activity of KCC2 will lead to an increase in intracellular chloride ion concentration, depolarization of neurons, an elevation in the excitability of the nervous system, and the occurrence of NP. Investigating the action mechanism of KCC2 is beneficial for comprehending the etiology, prophylaxis, and management of neuropathic pain. In this review, we will discuss the structure and function of KCC2 and its associated mechanisms that govern neuropathic pain, with the aim of offering novel insights into the prevention and treatment of this condition.
Communication Author:SI Yong-Yu , Email:siyongyu@kmmu.edu.cn