Long noncoding RNA (lncRNA): a target in neuropathic pain

ABSTRACT

Introduction: Current treatments for neuropathic pain are limited in part due to the incomplete understanding of its underlying mechanisms. Recent evidence reveals the dysregulated expression of long non-coding RNAs (lncRNAs) in the damaged nerve, dorsal root ganglion (DRG), and spinal cord dorsal horn following peripheral nerve injury. However, the role of the majority of lncRNAs in neuropathic pain genesis is still elusive. Unveiling the mechanisms of how lncRNAs participate in neuropathic pain may develop new strategies to prevent and/or treat this disorder.

Areas covered: This review focuses on the dysregulation of lncRNAs in the DRG, dorsal horn, and the injured nerves from preclinical models of neuropathic pain. We provide evidence of how peripheral nerve injury causes the dysregulation of lncRNAs in these pain-related regions. The potential mechanisms of how dysregulated lncRNAs contribute to the pathogenesis of neuropathic pain are discussed.

Expert opinion: The investigation on the role of the dysregulated lncRNAs in neuropathic pain might open up a novel avenue for therapeutic treatment of this disorder. However, current investigation is at the infancy stage, which challenges the translation of preclinical findings. More intensive studies on lncRNAs are required before the preclinical findings are translated into therapeutic management for neuropathic pain.

KEYWORDS:

• Long non-coding RNA
• neuropathic pain
• dorsal root ganglion
• spinal cord
• epigenetics
• RNA sequencing

Article highlights

• A large number of lncRNAs, including antisense RNAs and circular RNAs, are dysregulated in pain-related regions in the peripheral and central nerve systems following peripheral nerve injury.

• The Kcna2 antisense RNA participates in neuropathic pain through peripheral nerve injury-induced its upregulation, and consequently specific and selective silence of Kcan2 mRNA expression in the injured dorsal root ganglion.

• The role of the majority of dysregulated lncRNAs in neuropathic pain is still elusive and remains to be determined.

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Declaration of interest

The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Reviewer Disclosures

Peer reviewers on this manuscript have no relevant financial relationships or otherwise to disclose.

Additional information

Funding

This work was supported by NIH grants: R01NS094664, R01NS094224, and R01DA033390.