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Diabetic keratopathy is one of the common ocular complications of diabetes, and diabetic patients are often accompanied by changes in the morphological structure of the corneal endothelium.Oxidative stress, inflammation, apoptosis, glucose metabolism disorders, mitochondrial injury, and endoplasmic reticulum stress are the main mechanisms of the occurrence and progression of diabetic keratopathy.Studies have shown that advanced glycation end products can activate and induce the formation of a large number of reactive oxygen species (ROS), which in turn causes cell damage and even apoptosis.Mitochondria are the source of ROS, which will be damaged when a large amount of ROS accumulate, and mitochondrial autophagy will be formed when the body removes damaged mitochondria.Mitophagy refers to the process of eliminating aging, dysfunctional, damaged mitochondria through selective autophagy, which is a key mechanism for mitochondria to maintain function.The decrease in the level of mitophagy will lead to the destruction of the hexagonal structure of the diabetic corneal endothelium and its dysfunction, and upregulating the level of mitophagy can play a protective role on corneal endothelium in oxidative stress.The role of mitophagy in diabetic corneal endothelial lesions were reviewed in this article.
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Contributor Information
Department of Ophthalmology, Clinical Medical College of Shandong University, Jinan 250012, China
State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong First Medical University &
Shandong Academy of Medical Sciences, Qingdao 266071, China
State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong First Medical University &
Shandong Academy of Medical Sciences, Qingdao 266071, China