脊髓损伤是一种严重的中枢神经系统创伤性疾病，常见于坠落伤、交通事故、重物砸伤等，可造成机体损伤平面以下的运动、感觉和自主神经功能障碍。髓鞘相关抑制因子（MAI）在损伤的脊髓微环境中具有促进生长锥塌陷、抑制轴突再生的作用，是造成脊髓损伤难以修复的主要原因。髓鞘相关抑制因子类蛋白，如神经轴突生长抑制因子（Nogo）、少突胶质细胞髓鞘糖蛋白（OMgp）和髓鞘相关糖蛋白（MAG），及其受体蛋白如Nogo-A/Nogo-66受体1（NgR1）、配对免疫球蛋白样受体B（PirB）、鞘氨醇-1-磷酸受体（S1PR2），均是脊髓微环境中的重要调节因子，可通过影响神经元轴突生长的信号通路抑制脊髓损伤的修复过程。虽然目前脊髓损伤修复的机制还不清楚，但调节髓鞘相关抑制因子类蛋白及下游信号通路是脊髓损伤修复的重要治疗途径之一。我们通过本文对近年来MAI类蛋白及其受体在脊髓损伤修复中的作用进行综述，为脊髓损伤修复提供可探究的新靶点，并为脊髓损伤后的临床治疗提供更多思路。

Spinal cord injury is a traumatic disease, commonly seen in falling injuries, traffic accidents, heavy injuries, etc, which could cause motor, sensory and autonomic dysfunction below the level of spinal cord injury. Myelin-associated inhibitors play a role in promoting the collapse of growth cones and inhibiting axonal regeneration in the injured spinal cord microenvironment, which is the main reason for the difficult repair of spinal cord injury. Myelinassociated inhibitors (MAIs), such as neurite outgrowth inhibitor (Nogo), oligodendrocyte-myelin glycoprotein (OMgp) and myelin-associated glycoprotein (MAG), along with their receptor proteins, such as Nogo-A/Nogo-66 receptor 1 (NgR1), paired immunoglobulin-like receptor B (PirB), sphingosine-1-phosphate receptor 2 (S1PR2), are the important regulatory factors in the spinal cord microenvironment. They can inhibit therepair process of spinal cord injury by affecting the signaling pathway of neuron axon growth. Although the mechanism of spinal cord injury repair is still unclear, the regulation of myelin-related inhibitory factor proteins and downstream signaling pathways remain an important therapeutic approach for spinal cord injury. In this paper, the role of MAI proteins and their receptors in spinal cord injury repair in recent years were reviewed to provide a new target for spinal cord injury repair and provide more ideas for clinical treatment after spinal cord injury.