Redox homeostasis, oxidative stress and mitophagy
Redox homeostasis, oxidative stress and mitophagy
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DOI：
10.1016/j.mito.2020.01.002
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发表时间：
2020-03-01
期刊：
影响因子：
4.4
通讯作者：
Franco, Rodrigo
中科院分区：
文献类型：
--
作者：
Garza-Lombo, Carla;Pappa, Aglaia;Franco, Rodrigo
自噬是一种普遍存在的细胞成分降解或周转的稳态机制。线粒体自噬（mitophagy）的降解涉及许多生理过程，包括细胞的稳态，分化和衰老。在应激或损伤时，线粒体自噬防止受损线粒体的积累和导致氧化应激和细胞死亡的活性氧的稳态水平增加。许多人类疾病，特别是神经退行性疾病，都与线粒体自噬失调有关。本文就线粒体自噬调控的分子机制及其与氧化还原信号和氧化应激的关系进行综述。
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.