Chronic pain is a common and complex condition with multifactorial causes, and its development is closely associated with epigenetic regulation, particularly DNA methylation. DNA methylation and demethylation are mainly regulated by DNA methyltransferases (DNMTs) and ten-eleven translocation (TET) enzymes, which dynamically influence the expression of genes involved in nociceptive pathways, thereby modulating pro-nociceptive and anti-nociceptive signals.

Studies have shown that abnormal DNA methylation patterns are present in patients with various chronic pain conditions. These changes are associated with pain hypersensitivity, neuronal hyperexcitability, and increased inflammatory responses. Genome-wide analyses have also identified specific differentially methylated regions and genes that may serve as potential biomarkers for chronic pain, contributing to disease diagnosis and risk assessment.

Furthermore, during the transition from acute to chronic pain, DNA methylation undergoes rapid reprogramming, suggesting its involvement in the mechanisms underlying pain chronification. Therefore, understanding the temporal dynamics of DNA methylation at different stages is crucial for developing precise therapeutic strategies.

In the future, epigenetic therapies aimed at reversing abnormal DNA methylation patterns may become a promising approach for controlling chronic pain, providing more targeted options for pain management.

Reference:

1.Xiong, H.-Y., Wyns, A., Van Campenhout, J., Hendrix, J., De Bruyne, E., Godderis, L., Schabrun, S., Nijs, J., & Polli, A. (2024). International Journal of Molecular Sciences, 25(15), 8324.