# Targeting LncRNA‐Vof16: A Novel Therapeutic Strategy for Neuropathic Pain Relief

## TL;DR

This study identifies LncRNA-Vof16 as a potential new target for treating neuropathic pain by showing that its loss worsens pain while its overexpression reduces it.

## Contribution

The study introduces LncRNA-Vof16 as a novel therapeutic target for neuropathic pain.

## Key findings

- SNI caused downregulation of Vof16 in the spinal dorsal horn of rats.
- Disrupting Vof16 expression worsened hyperalgesia, while overexpression alleviated it.
- Vof16 appears to protect against neuropathic pain after nerve injury.

## Abstract

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.

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.

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.

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.

Graphical abstract showed that loss‐of‐function of LncRNA‐Vof16 (abbreviated as Vof16) aggravates neuronal hyperexcitability and hyperalgesia induced by spared nerve injury. On the contrary, gain‐of‐function of Vof16 holds the opposite and protective effects.