Epigenetic in human pain – an overview of experimental and clinical evidence

Epigenetics refers to the study of heritable changes in gene expression that are not due to alterations in the underlying DNA sequence. Evidence suggests that epigenetic mechanisms play a role in the development and persistence of pain conditions in humans. Several experimental studies have shown that epigenetic changes, such as DNA methylation, histone modifications, and non-coding RNA can regulate the expression of genes or their products involved in pain signaling pathways.
Experimental human evidence from Giordano et al. has shown how short pain stimulation in healthy subjects can induce changes in the profile of non-coding RNAs, such as microRNAs and lncRNAs, associated with pain pathways.
Clinical studies have also provided evidence of epigenetic changes in chronic pain patients. Altered DNA methylation of genes involved in pain mechanism has been demonstrated in patients with fibromyalgia or chronic low-back pain highlighting possible biomarkers for stratification of patients.
Giordano and colleagues have shown that alteration of preoperative circulating microRNAs and lncRNAs are linked to chronic pain after surgery. This suggests that these molecules could provide important information about a patient's prognosis. Moreover, computer models can identify pathways of regulation involving microRNAs and lncRNAs that are associated with pro-inflammatory cytokines known to play a role in the sensitization of nociceptors.
The field of epigenetics might provide a new understanding of the mechanisms underlying chronic pain in humans. Further research is needed to fully elucidate the role of epigenetic mechanisms in pain processing and to develop targeted epigenetic therapies for the treatment of chronic pain.