视网膜神经节细胞（RGCs）凋亡在视网膜退行性疾病中起到关键作用，在这个过程中Caspase-2信号通路激活至关重要。课题组前期研究发现在RGCs中，PIDD-CC参与了Caspase-2凋亡信号通路，并与RAIDD和Caspase-2存在相互作用。鉴于此，我们提出假说：PIDD-CC介导PIDD-CC/RAIDD/Caspase-2形成 PIDDosome三元复合物，并参与RGCs凋亡过程。课题组拟首先明确PIDD-CC参与RGCs凋亡过程；进一步通过检测三者表达、定位和相互作用，明确PIDDosome复合物的形成，及其在Caspase-2信号通路激活中的作用；随后在整体水平中，靶向干预RGCs中PIDDosome三元复合物的形成，分析其对视网膜形态和视觉行为学的影响。课题的研究结果可进一步阐明RGCs凋亡分子机制和调控网络，并为视网膜退行性疾病的防治提供新的理论基础和分子靶点。

The process of retinal ganglion cells (RGCs) apoptosis has been identified as the major contribution to retinal degenerative diseases, with the involvement of caspase-2 activation. Earlier study by our group has found the PIDD-CC recruits RAIDD and activates caspase-2. Therefore, we speculated that PIDD-CC participates RGCs apoptosis by the assembly of a PIDD-CC-RAIDD-caspase-2 complex. We aim to determine the involvement of PIDD-CC in RGCs apoptosis; investigate the expression, localization and interaction of PIDD-CC, RAIDD and caspase-2, as well as the role of the complex in caspase-2 activation; evaluate the effect of PIDDosome complex intervention on retinal morphology and visual behavior in optic nerve injury model. Our study will further clarify the molecular mechanisms and networks of the process of RGCs apoptosis; provide new theoretical basis and molecularly targeted therapy for the treatment of retinal degenerative diseases.