线粒体最初被认为是细胞的动力中心，并参与调节凋亡通路。然而，近期的研究表明，线粒体还在很大程度上参与先天性免疫反应。另外，Tfam和TOMs等已被证实参与运动介导线粒体质量控制的因子也被发现与先天性免疫反应的信号通路存在某种关联。因此，运动干预先天性免疫反应的若干途径之一可能是通过调控线粒体的结构、功能及相关信号分子得以实现的。在本研究中，我们拟通过建立细胞模型，对线粒体ROS水平进行干预，并分别敲除TOM70和Tfam两个关键分子；通过建立动物模型，对TOM70和Tfam分别进行过表达处理，并辅以运动训练干预，探讨线粒体DNA稳定性对cGAS-STING信号通路的调控机制，揭示线粒体输入机制（PIM）与MAVS间的联系，及其对下游NF-κB和IRF信号级联反应的影响，多部位、多水平探讨运动对线粒体介导先天性免疫反应的干预作用，揭示运动调控免疫系统的新机制。

Mitochondria were originally considered as the fuel center of cells, and were shown to be involved in apoptosis. However, recent evidence suggests that mitochondria also take part in innate immune response to a great extent. Besides, Tfam and TOMs, which have been demonstrated to be involved in exercise-mediated mitochondrial quality control, were also found to be related to certain signaling pathways of innate immune response. Therefore, it was hypothesized that one of the pathways that mediate exercise-induced innate immune response could be regulated by alterations of the structure, function and relating signaling molecules of mitochondria. In the present study, we will establish cell models, altering mitochondrial ROS level and knocking out the genes of TOM70 and Tfam, respectively. In addition, we will construct animal models, overexpressing TOM70 and Tfam, respectively and intervening with exercise training. We aim to investigate the role of DNA stability in cGAS-STING signaling pathway, reveal the association between PIM and MAVS, as well as the discuss the effect of above experimental manipulation on NF-κB and IRF signaling cascade. We hope that the effect of exercise on mitochondria-mediated innate immune response, and new mechanism of exercise regulating immune system could be explored by completion of this study.