Molecular Regulation Mechanisms and Interactions Between Reactive Oxygen Species and Mitophagy

被引：100
作者：
Fan, Pan [1 ]
Xie, Xing-Hui [1 ]
Chen, Chang-Hong [2 ]
Peng, Xin [1 ]
Zhang, Po [1 ]
Yang, Cheng [1 ]
Wang, Yun-Tao [1 ]
机构：
[1] Southeast Univ, Med Sch, Zhongda Hosp, Dept Spine Ctr, 87 Dingjiaqiao, Nanjing 210009, Jiangsu, Peoples R China
[2] Jiangyin Hosp Tradit Chinese Med, Dept Orthopaed Surg, Wuxi, Jiangsu, Peoples R China
来源：
DNA AND CELL BIOLOGY | 2019年 / 38卷 / 01期
关键词：
ROS; mitophagy; oxidative stress; mechanism; NF-KAPPA-B; MITOCHONDRIAL DYSFUNCTION; DAMAGED MITOCHONDRIA; AUTOPHAGIC CLEARANCE; OXIDATIVE STRESS; TARGET GENE; P38; MAPK; DEFECTIVE MITOCHONDRIA; DEPENDENT MITOPHAGY; MEDIATED MITOPHAGY;
D O I：
10.1089/dna.2018.4348
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The generation of reactive oxygen species (ROS) in response to oxidative stress has important effects on cell development, normal function, and survival. It may cause oxidative damage to intracellular macromolecular substances and mitochondria through several signaling pathways. However, the damaged mitochondria promote further ROS generation, creating a vicious cycle that can cause cellular injury. In addition, excessive ROS produced by damaged mitochondria can trigger mitophagy, a process that can scavenge impaired mitochondria and reduce ROS level to maintain stable mitochondrial function in cells. Therefore, mitophagy heaps maintain cellular homeostasis under oxidative stress. In this article, we review recent advances in cellular damage caused by excessive ROS, the mechanism of mitophagy, and the close relationship between ROS and mitophagy. This review provides a new perspective on therapeutic strategies for related diseases.
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收藏
页码：10 / 22
页数：13
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