粒体自噬
自噬
氧化应激
细胞生物学
线粒体
活性氧
氧化磷酸化
程序性细胞死亡
化学
平衡
生物
生物化学
细胞凋亡
作者
Carla Garza-Lombó,Aglaia Pappa,Mihalis I. Panayiotidis,Rodrigo Franco
出处
期刊:Mitochondrion
[Elsevier]
日期:2020-03-01
卷期号:51: 105-117
被引量:101
标识
DOI:10.1016/j.mito.2020.01.002
摘要
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.
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