CRMP2和电压门控离子通道:在神经性疼痛中的潜在作用。

Q4 Neuroscience
Neuronal signaling Pub Date : 2018-01-01 Epub Date: 2018-03-30 DOI:10.1042/NS20170220
Lindsey A Chew, Rajesh Khanna
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引用次数: 35

摘要

神经性疼痛对患者和整个社会来说都是一个巨大的负担。然而,神经性疼痛的治疗既复杂又具有挑战性,临床可用治疗的数量和质量有限加剧了这一问题。在这一阶段,功能失调的电压门控离子通道,特别是突触前n型电压门控钙通道(Cav2.2)和河豚毒素敏感的电压门控钠通道(Nav1.7),是神经性疼痛的病理生理基础,也是备受关注的治疗靶点。间接调节这些通道为神经性疼痛的治疗带来了希望。在这篇综述中,我们将重点关注塌陷反应介质蛋白2 (CRMP2),一个在电压门控离子通道运输中起重要作用的蛋白,并讨论靶向该蛋白的治疗潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

CRMP2 and voltage-gated ion channels: potential roles in neuropathic pain.

CRMP2 and voltage-gated ion channels: potential roles in neuropathic pain.

Neuropathic pain represents a significant and mounting burden on patients and society at large. Management of neuropathic pain, however, is both intricate and challenging, exacerbated by the limited quantity and quality of clinically available treatments. On this stage, dysfunctional voltage-gated ion channels, especially the presynaptic N-type voltage-gated calcium channel (Cav2.2) and the tetrodotoxin-sensitive voltage-gated sodium channel (Nav1.7), underlie the pathophysiology of neuropathic pain and serve as high profile therapeutic targets. Indirect regulation of these channels holds promise for the treatment of neuropathic pain. In this review, we focus on collapsin response mediator protein 2 (CRMP2), a protein with emergent roles in voltage-gated ion channel trafficking and discuss the therapeutic potential of targeting this protein.

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来源期刊
CiteScore
4.60
自引率
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14 weeks
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