The inhibition of miR-192-5p can promote nerve repair in rats with peripheral nerve injury (PNI) but the precise mechanisms underlying this effect remain unclear. Schwann cell (SC) autophagy mediated by autophagy-related gene (ATG) proteins has a key role in PNI but it is uncertain whether miR-192-5p affects the involvement of SC autophagy in PNI. In this study, we investigated the impact of methyltransferase-like protein 3 (METTL3)/miR-192-5p/ATG7 on SC autophagy in a rat PNI model and in an SC oxygen and glucose deprivation model. The results revealed that METTL3 stimulated miR-192-5p maturation via m6A methylation to depress ATG7 and SC autophagy and aggravate PNI. These findings provide a new target and potential basis for the treatment of patients with PNI.

中文翻译：

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METTL3 介导的 miR-192-5p 成熟以 ATG7 为靶点，以防止周围神经损伤中的雪旺细胞自噬。

抑制 miR-192-5p 可以促进周围神经损伤 (PNI) 大鼠的神经修复，但这种作用的确切机制仍不清楚。自噬相关基因 (ATG) 蛋白介导的雪旺细胞 (SC) 自噬在 PNI 中发挥关键作用，但 miR-192-5p 是否影响 SC 自噬在 PNI 中的参与尚不确定。在本研究中，我们研究了甲基转移酶样蛋白 3 (METTL3)/miR-192-5p/ATG7 在大鼠 PNI 模型和 SC 缺氧和葡萄糖剥夺模型中对 SC 自噬的影响。结果显示，METTL3通过m6A甲基化刺激miR-192-5p成熟，抑制ATG7和SC自噬，加重PNI。这些发现为PNI患者的治疗提供了新的靶点和潜在的基础。