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The Physiological Role of Mitophagy: New Insights into Phosphorylation Events

机译:线粒体的生理作用:磷酸化事件的新见解。

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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.
机译:线粒体在氧化磷酸化,脂肪酸氧化和细胞凋亡的调节中起着至关重要的作用。但是,该细胞器还会产生活性氧(ROS),不断对线粒体DNA,蛋白质和脂质造成氧化损伤,进而导致ROS的进一步产生。为了对抗这种氧化压力,线粒体拥有质量控制系统,其中包括抗氧化酶以及受损的线粒体DNA和蛋白质的修复或降解。如果氧化应激超过线粒体质量控制系统的能力,似乎自噬会降解受损的线粒体以维持细胞稳态。实际上,从酵母到哺乳动物的最新证据表明,线粒体的自噬依赖性降解(线粒体)有助于消除功能障碍,衰老或过量的线粒体。在本文中,我们描述了酵母和哺乳动物细胞中线粒体的分子过程和调控机制。

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