Parkinson’s disease (PD), as one of the complex neurodegenerative disorders, affects millions of aged people. Although the precise pathogenesis remains mostly unknown, a significant number of studies have demonstrated that mitochondrial dysfunction acts as a major role in the pathogeny of PD. Both nuclear and mitochondrial DNA mutations can damage mitochondrial integrity. Especially, mutations in several genes that PD-linked have a closed association with mitochondrial dysfunction (e.g., Parkin, PINK1, DJ-1, alpha-synuclein, and LRRK2). Parkin, whose mutation causes autosomal-recessive juvenile parkinsonism, plays an essential role in mitochondrial quality control of mitochondrial biogenesis, mitochondrial dynamics, and mitophagy. Therefore, we summarized the advanced studies of Parkin’s role in mitochondrial quality control and hoped it could be studied further as a therapeutic target for PD.

帕金森病 (PD) 作为一种复杂的神经退行性疾病，影响着数百万老年人。尽管确切的发病机制仍然未知，但大量研究表明线粒体功能障碍在 PD 的发病机制中起主要作用。核和线粒体 DNA 突变都会破坏线粒体的完整性。特别是，与 PD 相关的几个基因的突变与线粒体功能障碍密切相关（例如，Parkin、PINK1、DJ-1、α-突触核蛋白和 LRRK2）。Parkin 的突变导致常染色体隐性遗传的青少年帕金森综合征，在线粒体生物发生、线粒体动力学和线粒体自噬的线粒体质量控制中起着至关重要的作用。所以，