Mitochondrial Biology and Neurodegeneration Unit, Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.
Nat Cell Biol. 2024 Oct;26(10):1639-1651. doi: 10.1038/s41556-024-01513-9. Epub 2024 Oct 2.
Mitophagy mediated by the recessive Parkinson's disease genes PINK1 and Parkin responds to mitochondrial damage to preserve mitochondrial function. In the pathway, PINK1 is the damage sensor, probing the integrity of the mitochondrial import pathway, and activating Parkin when import is blocked. Parkin is the effector, selectively marking damaged mitochondria with ubiquitin for mitophagy and other quality-control processes. This selective mitochondrial quality-control pathway may be especially critical for dopamine neurons affected in Parkinson's disease, in which the mitochondrial network is widely distributed throughout a highly branched axonal arbor. Here we review the current understanding of the role of PINK1-Parkin in the quality control of mitophagy, including sensing of mitochondrial distress by PINK1, activation of Parkin by PINK1 to induce mitophagy, and the physiological relevance of the PINK1-Parkin pathway.
由隐性帕金森病基因 PINK1 和 Parkin 介导的线粒体自噬响应线粒体损伤以维持线粒体功能。在该途径中,PINK1 是损伤传感器,探测线粒体输入途径的完整性,并在输入受阻时激活 Parkin。Parkin 是效应物,通过泛素选择性地标记受损线粒体以进行线粒体自噬和其他质量控制过程。这种选择性的线粒体质量控制途径对于帕金森病中受影响的多巴胺神经元可能特别关键,其中线粒体网络广泛分布于高度分支的轴突树突中。在这里,我们回顾了 PINK1-Parkin 在线粒体自噬质量控制中的作用的现有认识,包括 PINK1 对线粒体窘迫的感应、PINK1 激活 Parkin 诱导线粒体自噬,以及 PINK1-Parkin 途径的生理相关性。