Noncoding RNAs: new players in chronic pain.
Noncoding RNAs: new players in chronic pain.
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DOI：
10.1097/aln.0000000000000265
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发表时间：
2014-08
期刊：
影响因子：
8.8
通讯作者：
Tao YX
中科院分区：
文献类型：
--
作者：
Lutz BM;Bekker A;Tao YX
慢性疼痛是一种常见的临床症状。由于我们对引发和维持慢性疼痛的分子机制缺乏了解，目前对这种疾病的治疗往往是不充分或无效的。外周炎症和神经损伤后背根神经节（DRG）初级感觉神经元基因表达的变化可能有助于慢性疼痛的发生。新发现的非编码RNA在基因调控机制中起着关键作用。最近的研究表明，外周伤害性刺激驱动非编码RNA的表达变化，这些变化与慢性疼痛条件下的疼痛超敏反应有关。本文首先介绍了外周炎症/神经损伤诱导的两种类型的非编码RNA，miRNA和Kcna 2反义RNA的表达变化，在疼痛相关区域，特别是在DRG中，外周炎症和神经损伤后的现有证据。然后，我们讨论如何外周伤害性刺激引起这种变化。最后，我们讨论了DRG miRNAs和Kcna 2 AS RNA的表达变化如何促进慢性疼痛的发展和维持的潜在机制。了解这些机制可能允许开发用于预防和/或治疗慢性疼痛的新的治疗策略。
Chronic pain is a common clinical symptom. Current treatments for this disorder are often inadequate or ineffective due to our deficient understanding of molecular mechanisms that trigger the initiation and maintenance of chronic pain. The changes in gene expression in primary sensory neurons of the dorsal root ganglion (DRG) following peripheral inflammation and nerve injury may contribute to chronic pain genesis. Newly identified noncoding RNAs play a critical role in the mechanism for gene regulation. 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 expression of two types of noncoding RNAs, miRNAs and Kcna2 antisense RNA, in pain-related regions, particularly in the DRG, after peripheral inflammation and nerve injury. We then discuss how peripheral noxious stimuli induce such changes. We finally discuss potential mechanisms of how expressional changes in DRG miRNAs and Kcna2 AS RNA contribute to the development and maintenance of chronic pain. Understanding of these mechanisms may allow the development of novel therapeutic strategies for preventing and/or treating chronic pain.