粒体自噬
氧化应激
线粒体
活性氧
细胞生物学
氧化磷酸化
生物
线粒体ROS
细胞内
生物化学
细胞凋亡
自噬
作者
Xiaobin Wen,Lixin Tang,Ruqing Zhong,Lei Liu,Liang Chen,Hongfu Zhang
出处
期刊:Antioxidants
[Multidisciplinary Digital Publishing Institute]
日期:2023-02-14
卷期号:12 (2): 480-480
被引量:29
标识
DOI:10.3390/antiox12020480
摘要
The mitochondrion is also a major site for maintaining redox homeostasis between reactive oxygen species (ROS) generation and scavenging. The quantity, quality, and functional integrity of mitochondria are crucial for regulating intracellular homeostasis and maintaining the normal physiological function of cells. The role of oxidative stress in human disease is well established, particularly in inflammatory bowel disease and gastrointestinal mucosal diseases. Oxidative stress could result from an imbalance between ROS and the antioxidative system. Mitochondria are both the main sites of production and the main target of ROS. It is a vicious cycle in which initial ROS-induced mitochondrial damage enhanced ROS production that, in turn, leads to further mitochondrial damage and eventually massive intestinal cell death. Oxidative damage can be significantly mitigated by mitophagy, which clears damaged mitochondria. In this review, we aimed to review the molecular mechanisms involved in the regulation of mitophagy and oxidative stress and their relationship in some intestinal diseases. We believe the reviews can provide new ideas and a scientific basis for researching antioxidants and preventing diseases related to oxidative damage.
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