During aging, the process of mitophagy, a system that allows the removal of dysfunctional mitochondria through lysosomal degradation, starts to malfunction. Because of this defect, damaged mitochondria are not removed correctly, and their decomposing components accumulate inside the cells. Dysfunctional mitochondria that are not removed by mitophagy produce high amounts of reactive oxygen species (ROS) and, thus, cause oxidative stress. Oxidative stress, in turn, is very harmful for the cells, neuronal cells, in particular. Consequently, the process of mitophagy plays a crucial role in mitochondria-related disease. Mitochondrial dysfunctions and oxidative stress are well-established factors contributing to Parkinson’s disease (PD), one of the most common neurodegenerative disorders. In this review, we report various known antioxidants for PD treatments and describe the stimulation of mitophagy process as a novel and exciting method for reducing oxidative stress in PD patients. We describe the different mechanisms responsible for mitochondria removal through the mitophagy process. In addition, we review the functional connection between mitophagy induction and reduction of oxidative stress in several in vitro models of PD and also agents (drugs and natural compounds) already known to be antioxidants and to be able to activate mitophagy. Finally, we propose that there is an urgent need to test the use of mitophagy-inducing antioxidants in order to fight PD.

中文翻译：

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线粒体自噬可以通过抗氧化作用对抗帕金森病

在衰老过程中，线粒体自噬（一种通过溶酶体降解去除功能失调的线粒体的系统）开始出现故障。由于这个缺陷，受损的线粒体没有被正确去除，它们的分解成分在细胞内积聚。没有被线粒体自噬去除的功能失调的线粒体会产生大量的活性氧 (ROS)，从而导致氧化应激。反过来，氧化应激对细胞，尤其是神经元细胞非常有害。因此，线粒体自噬过程在线粒体相关疾病中起着至关重要的作用。线粒体功能障碍和氧化应激是导致帕金森病 (PD) 的公认因素，帕金森病是最常见的神经退行性疾病之一。在本次审查中，我们报告了用于 PD 治疗的各种已知抗氧化剂，并将刺激线粒体自噬过程描述为一种减少 PD 患者氧化应激的新颖且令人兴奋的方法。我们描述了负责通过线粒体自噬过程去除线粒体的不同机制。此外，我们回顾了几种线粒体自噬诱导和氧化应激减少之间的功能联系。体外PD 模型以及已知为抗氧化剂并能够激活线粒体自噬的试剂（药物和天然化合物）。最后，我们建议迫切需要测试线粒体自噬诱导抗氧化剂的使用以对抗 PD。