Department of Anesthesiology & Critical Care Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Int J Mol Sci. 2024 Jun 23;25(13):6889. doi: 10.3390/ijms25136889.
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.
本文综述了表观遗传学在慢性颅面部神经病理性疼痛中的作用，为该领域提供了重要信息。因为慢性神经病理性疼痛的发生和维持过程中的表观遗传失调尚不完全清楚，特别是颅面部疼痛。我们注意到，报告的基因表达变化因神经损伤模型和报告的样本采集时间点而异。在我们的慢性神经病理性疼痛模型中，真正的慢性时间点为 10 周时，检查的功能基因群包括可能有助于抗炎、神经修复/再生和伤害感受的基因。本文还讨论了用表观遗传调节剂 LMK235 治疗后改变的基因。所有这些差异对于开发针对诊断的治疗方法都很关键，而且可能与治疗时机有关。本文再次强调了损伤后时间的相关性。
