Spinal cord injury (SCI), which is a leading cause of disability in modern society, commonly results from trauma. It has been reported that application of sciatic nerve conditioning injury plays a positive role in repairing the injury of the ascending spinal sensory pathway in laboratory animals. Because of the complexity of SCI and related ethics challenges, sciatic nerve conditioning injury cannot be applied in clinical therapy. Accordingly, it is extremely important to study its mechanism and develop replacement therapy. Based on empirical study and clinical trials, this article suggests that miR-142-3p is the key therapeutic target for repairing sensory function, based on the following evidence. Firstly, studies have reported that endogenous cAMP is the upstream regulator of 3 signal pathways that are partially involved in the mechanisms of sciatic nerve conditioning injury, promoting neurite growth. The regulated miR-142-3p can induce cAMP elevation via adenylyl cyclase 9 (AC9), which is abundant in dorsal root ganglia (DRG). Secondly, compared with gene expression regulation in the injured spinal cord, inhibition of microRNA (miRNA) in DRG is less likely to cause trauma and infection. Thirdly, evidence of miRNAs as biomarkers and therapeutic targets in many diseases has been reported. In this article we suggest, for the first time, imitating sciatic nerve conditioning injury, thereby enhancing central regeneration of primary sensory neurons via interfering with the congenerous upstream regulator AC9 of the 3 above-mentioned signal pathways. We hope to provide a new clinical treatment strategy for the recovery of sensory function in SCI patients.

Keywords: Cyclic AMP - metabolism, MicroRNAs - physiology, Spinal Cord Injuries - therapy