Wen Xiaobin, Tang Lixin, Zhong Ruqing, Liu Lei, Chen Liang, Zhang Hongfu
State Key Laboratory of Animal Nutrition, Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing 100193, China.
State Key Laboratory for Molecular Biology of Special Economic Animals, Institute of Special Animal and Plant Sciences, Chinese Academy of Agricultural Sciences, Changchun 130112, China.
Antioxidants (Basel). 2023 Feb 14;12(2):480. doi: 10.3390/antiox12020480.
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.
线粒体也是维持活性氧(ROS)生成与清除之间氧化还原稳态的主要场所。线粒体的数量、质量和功能完整性对于调节细胞内稳态及维持细胞正常生理功能至关重要。氧化应激在人类疾病中的作用已得到充分证实,尤其是在炎症性肠病和胃肠道黏膜疾病中。氧化应激可能源于ROS与抗氧化系统之间的失衡。线粒体既是ROS的主要产生部位,也是其主要作用靶点。这是一个恶性循环,最初由ROS诱导的线粒体损伤会增强ROS的产生,进而导致进一步的线粒体损伤,最终导致大量肠细胞死亡。线粒体自噬可清除受损线粒体,从而显著减轻氧化损伤。在本综述中,我们旨在综述线粒体自噬和氧化应激调节的分子机制及其在某些肠道疾病中的关系。我们相信这些综述可为研究抗氧化剂及预防与氧化损伤相关的疾病提供新思路和科学依据。