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Unlike acute pain, chronic pain lasts even after the period of initial stimulus such as inflammation or nerve damage. While acute pain is due to the peripheral component of pain circuitry, chronic pain is due to plastic changes throughout the somatosensory axis at molecular, cellular, system and cognitive levels. Chronic pain is a complex disorder, calls for clinical intervention but available medications are limited in efficacy or associated with severe side effects. The estimated financial burden of chronic pain is more than that of cardiac and diabetic problems together. Despite such severe societal impact and intense research efforts, current chronic pain treatment still relies on very few initially identified therapeutic targets. All these observations suggest a complex aetiology behind pain chronicity and call for novel approaches to better understand molecular machinery involved in chronic pain development and maintenance. The advent of sensitive genomic technologies enabled the discovery of several novel classes of non-coding RNAs (ncRNA), including microRNAs (miRNA). Over the last decade, an increasing number of studies reinforce the gene regulatory functions of each ncRNA species in health and disease. While the mechanism of action for miRNAs are relatively well understood, such knowledge for other ncRNAs is emerging. The current presentation will illustrate our previous and current studies to delineate functional significance and therapeutic potential of key miRNAs in chronic pain associated with cancer, neuropathy or diabetes. Insights into other ncRNAs as viable therapeutic targets for the treatment of chronic pain will be presented. Our current efforts in functional characterization of nociceptive classes via single-cell genomics will be discussed. |