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DNA Methylation and Non-Coding RNAs during Tissue-Injury Associated Pain

期刊

出版社

MDPI
DOI: 10.3390/ijms23020752

关键词

epigenetic; neuropathic pain; nociception; gene transcription; dorsal root ganglion; spinal dorsal horn; miRNA; siRNA; lncRNA; CpG islands

资金

  1. Indonesia Endowment Fund for Education
  2. Conselleria d'Innovacio, Universitats, Ciencia y Societat Digital de la Generalitat Valenciana [APOSTD/2021/150]
  3. Gobierno de Espana, Ministerio de Universidades
  4. UK Dementia Research Institute from UK DRI Ltd. - UK Medical Research Council
  5. Alzheimer's Society
  6. Alzheimer's Research UK
  7. Rosetrees, UK Medical Research Council

向作者/读者索取更多资源

This article summarizes and evaluates the effects of DNA methylation and non-coding RNA expression, two epigenetic mechanisms, on transcriptional modulation in nociceptive pathways during the development of tissue injury-associated pain. The potential of controlling these mechanisms as novel analgesic approaches and/or biomarkers of persistent pain is assessed.
While about half of the population experience persistent pain associated with tissue damages during their lifetime, current symptom-based approaches often fail to reduce such pain to a satisfactory level. To provide better patient care, mechanism-based analgesic approaches must be developed, which necessitates a comprehensive understanding of the nociceptive mechanism leading to tissue injury-associated persistent pain. Epigenetic events leading the altered transcription in the nervous system are pivotal in the maintenance of pain in tissue injury. However, the mechanisms through which those events contribute to the persistence of pain are not fully understood. This review provides a summary and critical evaluation of two epigenetic mechanisms, DNA methylation and non-coding RNA expression, on transcriptional modulation in nociceptive pathways during the development of tissue injury-associated pain. We assess the pre-clinical data and their translational implication and evaluate the potential of controlling DNA methylation and non-coding RNA expression as novel analgesic approaches and/or biomarkers of persistent pain.

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