Role of HDAC5 Epigenetics in Chronic Craniofacial Neuropathic Pain

TL;DR

This paper explores how epigenetic changes, specifically involving HDAC5, contribute to chronic craniofacial neuropathic pain and how these changes vary over time.

Contribution

The study highlights the role of HDAC5 and epigenetic modulators in chronic craniofacial pain, emphasizing the importance of timing in treatment.

Findings

Gene expression changes in chronic pain depend on the nerve injury model and time post-injury.

At 10 weeks post-injury, genes related to anti-inflammation, nerve repair, and nociception are altered.

Treatment with the epigenetic modulator LMK235 affects gene expression in chronic pain models.

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.

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