Autophagy is a ubiquitous homeostatic mechanism for the degradation or turnover of cellular components. Degradation of mitochondria via autophagy (mitophagy) is involved in a number of physiological processes including cellular homeostasis, differentiation and aging. Upon stress or injury, mitophagy prevents the accumulation of damaged mitochondria and the increased steady state levels of reactive oxygen species leading to oxidative stress and cell death. A number of human diseases, particularly neurodegenerative disorders, have been linked to the dysregulation of mitophagy. In this mini-review, we aimed to review the molecular mechanisms involved in the regulation of mitophagy and their relationship with redox signaling and oxidative stress.

中文翻译：

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氧化还原稳态、氧化应激和线粒体自噬

自噬是一种普遍存在的体内平衡机制，用于细胞成分的降解或周转。通过自噬 (mitophagy) 降解线粒体参与许多生理过程，包括细胞稳态、分化和衰老。在压力或受伤时，线粒体自噬可防止受损线粒体的积累和活性氧的稳态水平增加，从而导致氧化应激和细胞死亡。许多人类疾病，尤其是神经退行性疾病，都与线粒体自噬失调有关。在这篇小型综述中，我们旨在回顾参与调节线粒体自噬的分子机制及其与氧化还原信号和氧化应激的关系。