粒体自噬
活性氧
线粒体
细胞生物学
氧化应激
生物
细胞内
线粒体ROS
氧化磷酸化
程序性细胞死亡
生物化学
自噬
细胞凋亡
作者
Fan Pan,Xing-Hui Xie,Changhong Chen,Xin Peng,Po Zhang,Cheng Yang,Yuntao Wang
标识
DOI:10.1089/dna.2018.4348
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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