Abstract
AIMS: Neuropathic pain (NP) is a debilitating condition characterized by chronic pain resulting from nerve damage or lesion. Despite the ongoing efforts of clinically defining NP, its distinctive mechanisms that lead to various NP phenotypes remain unresolved. METHODS: Using a spared nerve injury (SNI) model, we investigated the mechanisms underlying the development of NP caused by injury in the peripheral nerves. With CRISPR-Cas9-mediated knockout and virus-mediated overexpression strategies, we investigated the role of LncRNA Vof16 (abbreviated as Vof16) during SNI-induced NP. RESULTS: Our results revealed that SNI led to the downregulation of Vof16 expression in spinal dorsal horn (SDH) of lumbar enlargement. This was evidently confirmed when we disrupted the expression of Vof16 in SNI rats of which we observed exacerbation of hyperalgesia; while overexpressing it alleviated the pain. CONCLUSION: Our findings suggest that Vof16 plays a crucial role in maintaining normal sensory function in healthy states and a protective shield against NP following peripheral nerve injury. We therefore propose Vof16 as a new therapeutic target for alleviating NP.