Role of Mitophagy in Regulating Intestinal Oxidative Damage.
Xiaobin WenLixin TangRuqing ZhongLei LiuLiang ChenHongfu ZhangPublished in: Antioxidants (Basel, Switzerland) (2023)
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.
Keyphrases
- reactive oxygen species
- oxidative stress
- cell death
- diabetic rats
- induced apoptosis
- cell cycle arrest
- dna damage
- ischemia reperfusion injury
- endothelial cells
- randomized controlled trial
- cell proliferation
- systematic review
- endoplasmic reticulum
- endoplasmic reticulum stress
- sensitive detection
- anti inflammatory
- pi k akt