Role of Mitophagy in Regulating Intestinal Oxidative Damage

被引:34
作者
Wen, Xiaobin [1 ]
Tang, Lixin [2 ]
Zhong, Ruqing [1 ]
Liu, Lei [1 ]
Chen, Liang [1 ]
Zhang, Hongfu [1 ]
机构
[1] Chinese Acad Agr Sci, Inst Anim Sci, State Key Lab Anim Nutr, Beijing 100193, Peoples R China
[2] Chinese Acad Agr Sci, Inst Special Anim & Plant Sci, State Key Lab Mol Biol Special Econ Anim, Changchun 130112, Peoples R China
基金
中国国家自然科学基金;
关键词
ROS; oxidative stress; mitophagy; PINK1-Parkin; intestinal damage;
D O I
10.3390/antiox12020480
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 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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页数:15
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