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非编码 RNA:慢性疼痛的新角色。

Noncoding RNAs: new players in chronic pain.

机构信息

From the Department of Anesthesiology, Rutgers Graduate School of Biomedical Sciences (B.M.L.), Department of Anesthesiology (A.B.), and Departments of Anesthesiology, Cell Biology and Molecular Medicine, Pharmacology and Physiology, and Neurology and Neuroscience (Y.-X.T.), New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, New Jersey.

出版信息

Anesthesiology. 2014 Aug;121(2):409-17. doi: 10.1097/ALN.0000000000000265.

DOI:10.1097/ALN.0000000000000265
PMID:24739997
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4110167/
Abstract

Chronic pain, a common clinical symptom, is often treated inadequately or ineffectively in part due to the incomplete understanding of molecular mechanisms that initiate and maintain this disorder. Newly identified noncoding RNAs govern gene expression. Recent studies have shown that peripheral noxious stimuli drive expressional changes in noncoding RNAs and that these changes are associated with pain hypersensitivity under chronic pain conditions. This review first presents current evidence for the peripheral inflammation/nerve injury-induced change in the expression of two types of noncoding RNAs, microRNAs, and Kcna2 antisense RNA, in pain-related regions, particularly in the dorsal root ganglion. The authors then discuss how peripheral noxious stimuli induce such changes. The authors finally explore potential mechanisms of how expressional changes in dorsal root ganglion microRNAs and Kcna2 antisense RNA contribute to the development and maintenance of chronic pain. An understanding of these mechanisms may propose novel therapeutic strategies for preventing and/or treating chronic pain.

摘要

慢性疼痛是一种常见的临床症状,部分原因是对引发和维持这种疾病的分子机制的不完全了解,导致其治疗往往不充分或无效。新发现的非编码 RNA 控制基因表达。最近的研究表明,外周伤害性刺激会导致非编码 RNA 的表达发生变化,而这种变化与慢性疼痛条件下的疼痛敏感性增加有关。这篇综述首先介绍了目前关于两种类型的非编码 RNA(microRNA 和 Kcna2 反义 RNA)在与疼痛相关的区域(特别是背根神经节)中,在外周炎症/神经损伤诱导的表达变化的证据。作者随后讨论了外周伤害性刺激如何诱导这种变化。作者最后探讨了背根神经节 microRNA 和 Kcna2 反义 RNA 表达变化如何导致慢性疼痛的发展和维持的潜在机制。了解这些机制可能为预防和/或治疗慢性疼痛提出新的治疗策略。

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本文引用的文献

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miR-7a alleviates the maintenance of neuropathic pain through regulation of neuronal excitability.miR-7a 通过调节神经元兴奋性缓解神经性疼痛的维持。
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A long noncoding RNA contributes to neuropathic pain by silencing Kcna2 in primary afferent neurons.一种长非编码 RNA 通过沉默初级传入神经元中的 Kcna2 来促进神经性疼痛。
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