随着交通事业的日益发展，脊髓损伤越来越常见，也是脊柱外科的严重并发症，严重威胁人类健康。因此，脊髓损伤一直是当今医学界的研究热点，但具体机制及病理过程尚未被明确阐明。我们前次国家自然科学基金研究结果表明：线粒体途径介导的神经细胞凋亡在脊髓损伤过程中发挥重要作用。本项目拟在既往研究基础上，通过应用Drp1小分子特异性抑制剂Mdivi-1及Drp1基因敲除小鼠，探讨脊髓损伤过程中Drp1丝氨酸637位点去磷酸化激活对Bax线粒体特异性移位的影响，同时阐述Bax特异性移位至线粒体并插入线粒体外膜活化后对自噬的调节作用。一旦证实，本研究将在理论上首次阐述脊髓损伤时BAX线粒体移位机制及其对自噬的影响，并创新地串联神经细胞凋亡及自噬两大病理机制，为脊髓损伤时线粒体功能的研究开辟新视野。在临床上，为早期治疗急性脊髓损伤提供新思路、新方法。

With the increasing development of transportation, spinal cord injury has been the most common and serious complication that threatens human's health in clinical spinal surgery. The pathogenesis and pathological process of spinal injury has been the key issue in medical community, however, the mechanism remains unclear. Our findings in pervious National Nature Science Foundation showed that mitochondria-mediated apoptosis played a pivotal role after spinal injury. Based on the pervious research, our objective is probing into the influence of dephosphorylation of Drp1 at ser637 on the translocation of BAX to mitochondria after spinal injury, by applying the drp1 inhibitor Mdivi-1 and Drp1 gene knock-out mice. In addition, we will discuss the mechanism of autophagy regulated by special translocation of Bax to mitochondria. Once demonstrated, we will not only define the mechanism of translocation, insertion and activity of Bax, and link mitochondria-mediated apoptosis and autophagy in theory. We will break a new field for the research of function of mitochondria after spinal cord injury, and provide the new therapy for the spinal cord injury in clinical.