Abstract
Chronic pain, a severe public health issue, affects the quality of life of patients and results in a major socioeconomic burden. Only limited drug treatments for chronic pain are available, and they have insufficient efficacy. Recent studies have found that the expression of long non-coding RNAs (lncRNAs) is dysregulated in various chronic pain models, including chronic neuropathic pain, chronic inflammatory pain, and chronic cancer-related pain. Studies have also explored the effect of these dysregulated lncRNAs on the activation of microRNAs, inflammatory cytokines, and so on. These mechanisms have been widely demonstrated to play a critical role in the development of chronic pain. The findings of these studies indicate the significant roles of dysregulated lncRNAs in chronic pain in the dorsal root ganglion and spinal cord, following peripheral or central nerve lesions. This review summarizes the mechanism underlying the abnormal expression of lncRNAs in the development of chronic pain induced by peripheral nerve injury, diabetic neuropathy, inflammatory response, trigeminal neuralgia, spinal cord injury, cancer metastasis, and other conditions. Understanding the effect of lncRNAs may provide a novel insight that targeting lncRNAs could be a potential candidate for therapeutic intervention in chronic pain.
Highlights
Chronic pain is an extremely prevalent healthcare issue that affects the quality of life of patients, resulting in an annual financial impact (van Hecke et al, 2014; Hamood et al, 2018)
Since numerous long non-coding RNAs (lncRNAs) are involved, we have summarized the following points: (1) Most lncRNAs interacted with miRNAs, and Metastasis-associated lung adenocarcinoma transcript1 (MALAT1) and X-inactive specific transcript (XIST) were the most common among these lncRNAs. miRNA downregulation triggered by these lncRNAs could influence the downstream mechanism and induce mechanical and cold hypersensitivity and the symptoms of peripheral nerve injury (PNI)-associated chronic neuropathic pain (CNP)
MALAT1 expression was increased in the L4-L6 spinal cord of male constriction injury (CCI) rats (Ma et al, 2020), while its expression was reduced in the C5-T1 spinal cord of male complete brachial plexus avulsion rats (Meng et al, 2019)
Summary
Chronic pain is an extremely prevalent healthcare issue that affects the quality of life of patients, resulting in an annual financial impact (van Hecke et al, 2014; Hamood et al, 2018). PNI can cause excitability of the primary sensory ganglia or the spinal cord in the nervous system (Tsuda et al, 2009), which plays a role in pain-signaling transmission Most animal models, such as those of chronic constriction injury (CCI), spinal nerve ligation (SNL), and spared sciatic nerve injury (SNI), have been used to investigate the relationship between lncRNAs and CNP in the nervous system (Table 1 and Figure 2). Changes in the levels of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) have been found in most PNI models (Li Z. et al, 2020; Pan et al, 2020), indicating that lncRNA-mediated CNP development may be involved in neuroinflammation. MALAT1 expression was increased in the L4-L6 spinal cord of male CCI rats (Ma et al, 2020), while its expression was reduced in the C5-T1 spinal cord of male complete brachial plexus avulsion rats (Meng et al, 2019). (3) Owing to the sex difference in pain sensitivity (Fullerton et al, 2018), clinical and experimental findings have suggested that women are more sensitive to pain than men (Fillingim et al, 2009). lncRNA XIST, which mediates
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