关键词: cold allodynia miRNA nerve injury neural regeneration trigeminal

Mesh : Neuralgia / genetics Epigenesis, Genetic Animals Humans Histone Deacetylases / genetics metabolism Chronic Pain / genetics Facial Pain / genetics

来  源:   DOI:10.3390/ijms25136889   PDF(Pubmed)

Abstract:
The information provided from the papers reviewed here about the role of epigenetics in chronic craniofacial neuropathic pain is critically important because epigenetic dysregulation during the development and maintenance of chronic neuropathic pain is not yet well characterized, particularly for craniofacial pain. We have noted that gene expression changes reported vary depending on the nerve injury model and the reported sample collection time point. At a truly chronic timepoint of 10 weeks in our model of chronic neuropathic pain, functional groupings of genes examined include those potentially contributing to anti-inflammation, nerve repair/regeneration, and nociception. Genes altered after treatment with the epigenetic modulator LMK235 are discussed. All of these differentials are key in working toward the development of diagnosis-targeted therapeutics and likely for the timing of when the treatment is provided. The emphasis on the relevance of time post-injury is reiterated here.
摘要:
本文综述的关于表观遗传学在慢性颅面神经性疼痛中的作用的论文提供的信息至关重要,因为在慢性神经性疼痛的发展和维持过程中的表观遗传失调尚未得到很好的表征。尤其是颅面疼痛.我们已经注意到,所报道的基因表达变化根据神经损伤模型和所报道的样品收集时间点而变化。在我们的慢性神经性疼痛模型中,在10周的真正慢性时间点,所检查的基因功能分组包括那些可能有助于抗炎的基因,神经修复/再生,和伤害性。讨论了用表观遗传调节剂LMK235治疗后改变的基因。所有这些差异都是开发诊断靶向疗法的关键,并且可能是提供治疗的时机。这里重申了对受伤后时间相关性的强调。
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