Redox homeostasis, oxidative stress and mitophagy

被引：108

作者：

Garza-Lombo, Carla ^{[1
,2
]}

Pappa, Aglaia ^{[3
]}

Panayiotidis, Mihalis, I ^{[4
]}

Franco, Rodrigo ^{[1
,2
]}

机构：

[1] Univ Nebraska, Redox Biol Ctr, 114 VBS 0905, Lincoln, NE 68583 USA

[2] Univ Nebraska, Sch Vet Med & Biomed Sci, 114 VBS 0905, Lincoln, NE 68583 USA

[3] Democritus Univ Thrace, Dept Mol Biol & Genet, Alexandroupolis 68100, Greece

[4] Northumbria Univ, Dept Appl Sci, Newcastle Upon Tyne NE1 8ST, Tyne & Wear, England

来源：

MITOCHONDRION | 2020年 / 51卷

基金：

美国国家卫生研究院;

关键词：

Autophagy; Mitochondrial dynamics; Fission; Fusion; REGULATES MITOCHONDRIAL DYNAMICS; PROTEIN-TYROSINE PHOSPHATASES; TRANSCRIPTION FACTOR NRF2; S-NITROSYLATION; ULK1; COMPLEX; NITRIC-OXIDE; PARKINSONS-DISEASE; UBIQUITIN CHAINS; BNIP3; PROTEIN; MTOR PATHWAY;

D O I：

10.1016/j.mito.2020.01.002

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

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.

引用

页码：105 / 117

页数：13

共 218 条

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