Hirota Yuko, Kang Dongchon, Kanki Tomotake
Department of Clinical Chemistry and Laboratory Medicine, Kyushu University Graduate School of Medical Sciences, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
Int J Cell Biol. 2012;2012:354914. doi: 10.1155/2012/354914. Epub 2012 Mar 7.
Mitochondria play an essential role in oxidative phosphorylation, fatty acid oxidation, and the regulation of apoptosis. However, this organelle also produces reactive oxygen species (ROS) that continually inflict oxidative damage on mitochondrial DNA, proteins, and lipids, which causes further production of ROS. To oppose this oxidative stress, mitochondria possess quality control systems that include antioxidant enzymes and the repair or degradation of damaged mitochondrial DNA and proteins. If the oxidative stress exceeds the capacity of the mitochondrial quality control system, it seems that autophagy degrades the damaged mitochondria to maintain cellular homeostasis. Indeed, recent evidence from yeast to mammals indicates that the autophagy-dependent degradation of mitochondria (mitophagy) contributes to eliminate dysfunctional, aged, or excess mitochondria. In this paper, we describe the molecular processes and regulatory mechanisms of mitophagy in yeast and mammalian cells.
线粒体在氧化磷酸化、脂肪酸氧化及细胞凋亡调控中发挥着至关重要的作用。然而，这种细胞器也会产生活性氧（ROS），持续对线粒体DNA、蛋白质和脂质造成氧化损伤，进而导致更多ROS的产生。为对抗这种氧化应激，线粒体拥有质量控制系统，包括抗氧化酶以及对受损线粒体DNA和蛋白质的修复或降解。如果氧化应激超过了线粒体质量控制系统的能力，自噬似乎会降解受损线粒体以维持细胞内稳态。事实上，最近从酵母到哺乳动物的证据表明，自噬依赖性的线粒体降解（线粒体自噬）有助于清除功能失调、老化或多余的线粒体。在本文中，我们描述了酵母和哺乳动物细胞中线粒体自噬的分子过程和调控机制。
