自噬通过BDNF/TrkB信号通路对脊髓损伤的保护作用

脊髓型颈椎病(cervical spondylotic myelopathy, CSM)是临床常见病、多发病,由该病引起的脊髓受损而产生的脊髓功能障碍是其最常见的临床特征。在脊髓损伤中,多种因素能通过自噬相关信号通路而激活自噬,适度的自噬可以对脊髓损伤起到神经保护作用,而增加细胞存活率、恢复和增加自噬通量可以改善损伤后的脊髓功能的恢复;在CSM脊髓损伤中,脑源性神经营养因子(brain derived neurotrophic factor, BDNF)与其受体原肌球蛋白受体激酶B(tropomyosin receptor kinase B, TrkB)及其相关通路是参与保护神经细胞的重要途径之一,细胞自噬在这一过程中起到了重要的调节作用。本文通过阐释自噬与BDNF/TrkB信号通路在CSM过程中的作用及其对脊髓损伤的保护机制,以期对基础研究及临床研究提供理论支持。

Protective effect of autophagy on spinal cord injury through BDNF/Trk B signaling pathway

Cervical spondylotic myelopathy(CSM) is a common and frequently-occurring disease. Spinal cord dysfunction caused by spinal cord damage caused by this disease is its most common clinical feature. In spinal cord injury, multiple factors can activate autophagy through autophagy-related signaling pathways. Moderate autophagy can protect neurons from spinal cord injury, while increasing cell survival rate, restoring and increasing autophagy flux can improve post-injury. Neurotrophic factor BDNF and its receptor TrkB and its related pathways in CSM spinal cord injury are one of the important ways to participate in the protection of nerve cells. Autophagy plays an important regulatory role in this process. This article provides theoretical support for basic research and clinical research by elucidating the role of autophagy and BDNF/TrkB signaling pathway in CSM and its protective mechanism against spinal cord injury.