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周围神经性疼痛:背根神经节神经元的实验模型与潜在治疗靶点。

Peripheral Neuropathic Pain: From Experimental Models to Potential Therapeutic Targets in Dorsal Root Ganglion Neurons.

机构信息

Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei 10051, Taiwan.

Department of Life Science, College of Life Science, National Taiwan University, Taipei 10617, Taiwan.

出版信息

Cells. 2020 Dec 21;9(12):2725. doi: 10.3390/cells9122725.

DOI:10.3390/cells9122725
PMID:33371371
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7767346/
Abstract

Neuropathic pain exerts a global burden caused by the lesions in the somatosensory nerve system, including the central and peripheral nervous systems. The mechanisms of nerve injury-induced neuropathic pain involve multiple mechanisms, various signaling pathways, and molecules. Currently, poor efficacy is the major limitation of medications for treating neuropathic pain. Thus, understanding the detailed molecular mechanisms should shed light on the development of new therapeutic strategies for neuropathic pain. Several well-established in vivo pain models were used to investigate the detail mechanisms of peripheral neuropathic pain. Molecular mediators of pain are regulated differentially in various forms of neuropathic pain models; these regulators include purinergic receptors, transient receptor potential receptor channels, and voltage-gated sodium and calcium channels. Meanwhile, post-translational modification and transcriptional regulation are also altered in these pain models and have been reported to mediate several pain related molecules. In this review, we focus on molecular mechanisms and mediators of neuropathic pain with their corresponding transcriptional regulation and post-translational modification underlying peripheral sensitization in the dorsal root ganglia. Taken together, these molecular mediators and their modification and regulations provide excellent targets for neuropathic pain treatment.

摘要

神经病理性疼痛是由躯体感觉神经系统(包括中枢和外周神经系统)的损伤引起的全球性负担。神经损伤引起的神经病理性疼痛的机制涉及多种机制、多种信号通路和分子。目前,药物治疗神经病理性疼痛的疗效不佳是主要限制因素。因此,了解详细的分子机制应该为开发治疗神经病理性疼痛的新治疗策略提供启示。已经建立了几种可靠的体内疼痛模型,用于研究周围神经病理性疼痛的详细机制。疼痛的分子介质在各种形式的神经病理性疼痛模型中被差异化地调节;这些调节剂包括嘌呤能受体、瞬时受体电位受体通道以及电压门控钠和钙通道。同时,这些疼痛模型中的翻译后修饰和转录调控也发生了改变,并被报道调节了几种与疼痛相关的分子。在这篇综述中,我们重点关注了神经病理性疼痛的分子机制和介质,以及它们在背根神经节外周敏化中的相应转录调控和翻译后修饰。综上所述,这些分子介质及其修饰和调控为神经病理性疼痛的治疗提供了极好的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dee/7767346/c2725df7e38c/cells-09-02725-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dee/7767346/c2725df7e38c/cells-09-02725-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dee/7767346/c2725df7e38c/cells-09-02725-g001.jpg

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