The role of non-coding RNAs in neuropathic pain.

IF 2.9 4区 医学 Q2 PHYSIOLOGY
Xiuying He, Huisi Yang, Yuexiang Zheng, Xiaoming Zhao, Tinghua Wang
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引用次数: 0

Abstract

Neuropathic pain (NPP) is a refractory pain syndrome, caused by damage or disease of the somatosensory nervous system and characterized by spontaneous pain, hyperalgesia, abnormal pain and sensory abnormality. Non-coding RNAs (ncRNAs), including microRNA (miRNA), long non-coding RNA (lncRNA), circular RNA (circRNA) and Piwi interacting RNA (piRNA), play a notable role in initiation and maintenance of NPP. In this review, we summarize the role of ncRNAs in NPP and their underlaying mechanism. Generally, ncRNAs are interacted with mRNA, protein or DNA to regulate the molecules and signals assciated with neuroinflammation, ion channels, neurotrophic factors and others, and then involved in the occurrence and development of NPP. Therefore, this review not only contributes to deepen our understanding of the pathophysiological mechanism of NPP, but also provides theoretical basis for the development of new therapy strategies for this disorder.

Abstract Image

非编码 RNA 在神经性疼痛中的作用。
神经病理性疼痛(NPP)是一种难治性疼痛综合征,由躯体感觉神经系统损伤或疾病引起,以自发性疼痛、痛觉亢进、疼痛异常和感觉异常为特征。非编码 RNA(ncRNA),包括微 RNA(miRNA)、长非编码 RNA(lncRNA)、环状 RNA(circRNA)和 Piwi 交互 RNA(piRNA),在 NPP 的启动和维持中发挥着显著作用。在这篇综述中,我们总结了 ncRNA 在 NPP 中的作用及其内在机制。一般来说,ncRNA 与 mRNA、蛋白质或 DNA 相互作用,调控与神经炎症、离子通道、神经营养因子等相关的分子和信号,进而参与 NPP 的发生和发展。因此,这篇综述不仅有助于加深我们对 NPP 病理生理机制的理解,还为开发治疗该疾病的新策略提供了理论依据。
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来源期刊
CiteScore
8.80
自引率
2.20%
发文量
121
审稿时长
4-8 weeks
期刊介绍: Pflügers Archiv European Journal of Physiology publishes those results of original research that are seen as advancing the physiological sciences, especially those providing mechanistic insights into physiological functions at the molecular and cellular level, and clearly conveying a physiological message. Submissions are encouraged that deal with the evaluation of molecular and cellular mechanisms of disease, ideally resulting in translational research. Purely descriptive papers covering applied physiology or clinical papers will be excluded. Papers on methodological topics will be considered if they contribute to the development of novel tools for further investigation of (patho)physiological mechanisms.
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