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氧化还原平衡、氧化应激和线粒体自噬。

Redox homeostasis, oxidative stress and mitophagy.

机构信息

Redox Biology Center and School of Veterinary Medicine and Biomedical Sciences, University of Nebraska-Lincoln, Lincoln, NE 68583, United States.

Department of Molecular Biology & Genetics, Democritus University of Thrace, Alexandroupolis 68100, Greece.

出版信息

Mitochondrion. 2020 Mar;51:105-117. doi: 10.1016/j.mito.2020.01.002. Epub 2020 Jan 20.

Abstract

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.

摘要

自噬是一种普遍存在的细胞内成分降解或更新的内稳态机制。通过自噬(mitophagy)降解线粒体参与了许多生理过程,包括细胞内稳态、分化和衰老。在应激或损伤时,自噬可以防止受损线粒体的积累和活性氧(reactive oxygen species)稳态水平的增加,从而导致氧化应激和细胞死亡。许多人类疾病,特别是神经退行性疾病,都与自噬的失调有关。在这篇综述中,我们旨在回顾参与自噬调节的分子机制及其与氧化还原信号和氧化应激的关系。

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