线粒体自噬指细胞通过自噬机制选择性除去损伤或多余的线粒体。真核生物通过线粒体自噬调控线粒体质量，维持供能细胞器的功能。大量研究表明，帕金森病相关基因PINK1和parkin可通过线粒体自噬参与并维持线粒体功能。PINK1与parkin能协同特异性识别损伤的线粒体，PINK1作为线粒体质量调控的探测器被活化，此过程中泛素化酶和去泛素化酶对维持parkin活性及线粒体自噬的效率有重要作用。本文主要总结PINK1/parkin通路在线粒体自噬中的功能与作用。

Mitophagy is a special version of autophagy which eliminates damaged or redundant mitochondria effectively and selectively. Eukaryotes conduct mitochondrial quality control via mitophagy to maintain the function of the power-generating organelles. Recently, a series of studies have demonstrated that two Parkinson’s disease-related genes, PINK1 and parkin, were involved in mitophagy. Parkin and PINK1 cooperate with each other to recognize damaged mitochondria specifically. Particularly, ubiquitin and deubiquitinases play essential roles in modulating parkin activity and mitophagy efficiency. Here we introduce and review the recent studies on PINK1/parkin pathway in mitophagy.