[综述]
[综述]
糖尿病角膜病变是常见的糖尿病眼部并发症之一，糖尿病患者多伴有角膜内皮形态结构的改变。氧化应激、炎症、细胞凋亡、糖脂代谢紊乱、线粒体损伤和内质网应激是糖尿病角膜病变发生和发展的主要机制。研究表明，晚期糖基化终末产物可激活并诱发生成大量活性氧簇(ROS)，进而造成细胞的损伤，甚至凋亡。线粒体是产生ROS的源泉，大量的ROS累积会造成线粒体损伤，机体清除损伤的线粒体，形成线粒体自噬。线粒体自噬是指通过选择性自噬消除衰老、功能障碍、损伤的线粒体的过程，这是线粒体维持功能的关键机制。而线粒体自噬水平下降会导致糖尿病角膜内皮的六边形结构被破坏及功能障碍，上调线粒体自噬水平能够在氧化应激中对角膜内皮起到保护作用。本文主要对线粒体自噬在糖尿病角膜内皮病变中的作用进行综述。
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.
陈晨,周庆军,谢立信. 线粒体自噬在糖尿病角膜内皮病变中的作用[J]. 中华实验眼科杂志,2022,40(12)：1181-1185.
DOI:10.3760/cma.j.cn115989-20191211-00539版权归中华医学会所有。
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