线粒体功能障碍与原发性开角型青光眼的研究进展  

Is glaucoma a mitochondrial neurodegenerative disease

作　　者：章征[1] 马建民 王宁利[1] 

机构地区：[1]首都医科大学附属北京同仁医院北京同仁眼科中心、北京市眼科研究所北京市眼科学与视觉科学重点实验室,100730

出　　处：《中华眼科杂志》2016年第9期714-717,共4页Chinese Journal of Ophthalmology

摘　　要：由于视网膜神经节细胞的结构及能量需求特殊，因此其对线粒体的功能障碍非常敏感。编码线粒体蛋白质的线粒体DNA和核DNA改变会影响线粒体的结构和功能，可以导致原发性开角型青光眼。本文将结合青光眼的主要危险因素（高眼压及高龄），分析其与线粒体功能障碍之间的相关性；并在线粒体功能障碍可导致青光眼视神经损伤的理论基础上，探讨新的旨在优化线粒体功能的治疗方法。（中华眼科杂志，2016，52：714-717）The retinal ganglion cell, due to peculiar structural and energetic constraints, appears acutely susceptible to mitochondrial dysfunction. Emerging evidence suggests that changes in the mitochondrial DNA （mtDNA） and in nuclear DNA genes that encode mitochondrial proteins may influence mitochondrial structure and function and, therefore, contribute to the pathogenesis of primary open angle glaucoma. As the main glaucoma risk factors are elevated intraocular pressure and older age, we discuss their relationship with mitochondrial dysfunction. If the contribution of mitochondrial dysfunction to glaucoma pathogenesis is further established, emerging therapies aiming to optimize mitochondrial function represent potential clinical treatments.

关 键 词：青光眼 开角型 线粒体疾病 视网膜神经节细胞 

分 类 号：R775.2[医药卫生—眼科]