缺氧是牙髓炎症发生发展过程中的一种重要病理现象。线粒体自噬是指细胞受损时，功能不完全的线粒体被选择性包裹进自噬体而降解清除，是维持胞内环境稳定和保证线粒体网络功能完整的重要机制，与缺氧损伤关系密切。FUNDC1是与缺氧紧密相关的线粒体自噬相关因子，研究显示Calnexin和DRP1协同FUNDC1调控线粒体自噬。现已证实牙髓细胞自噬与缺氧、炎症和老化等有关。申请人前期研究发现脂多糖可诱导牙髓细胞自噬，FUNDC1在牙髓细胞中表达并可被抑制。本课题拟研究缺氧环境下人牙髓细胞线粒体自噬的改变与FUNDC1在其中的调控作用以及Calnexin和DRP1在该过程中对FUNDC1的协同机制。本项目从细胞器出发，着眼于细胞超微结构，旨在阐明炎症早期，缺氧环境下人牙髓细胞线粒体自噬发生发展过程中FUNDC1及Calnexin、DRP1在其中的作用，为研究牙髓组织损伤时的修复机制提供理论依据和新的切入点。

Hypoxia is significant pathological phenomena during procedure of pulpitis. Mitophagy, a process that dysfunctional mitochondrial is selectively wrapped in autolysosome and degrade when cells are damaged, is a significant mechanism to maintain intracellular environment stability and guarantee the complete mitochondrial network function and is associated with hypoxia. FUNDC1 is a mitophagy factor related to hypoxia. It has been confirmed that FUNDC1 regulate mitophagy with calnexin and DRP1. Autophagy in human dental pulp cells has been verified to be responsive to hypoxia, inflammation and aging. We had detected that LPS up-regulated autophagy of hDPCs and FUNDC1 expressed by dental pulp cells can be suppressed. This project determines mitophagy induced by hypoxia in human dental pulp cells and the role of FUNDC1 in the mechanism with calnexin and DRP1. This study may provide evidence from organelles and ultra structure to understand procedure mitophagy in human dental pulp cells under hypoxia and the mechanisms involved by FUNDC1, calnexin and DRP1. Thus, it may reveal novel theoretical basis and entry point for clinical management of damaged pulp tissue.