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[线粒体功能障碍与辅酶Q10在青光眼患者中的作用]

[Mitochondrial Dysfunctions and Role of Coenzyme Q10 in Patients with Glaucoma].

作者信息

Erb Carl, Konieczka Katarzyna

机构信息

Augenklinik am Wittenbergplatz, Berlin.

Augenheilkunde, Universität Basel, Schweiz.

出版信息

Klin Monbl Augenheilkd. 2018 Feb;235(2):157-162. doi: 10.1055/s-0044-101618. Epub 2018 Feb 15.

Abstract

Mitochondrial function is closely linked to numerous aspects of eye health. Imbalance between the creation of energy and the development of reactive oxygen species (ROS) seems to be the cause of the development of mitochondrial dysfunctions. As a result of this energy deficit, the level of oxidative stress in the eye tissues increases, leading to numerous ophthalmic impairments. It is important to distinguish between primary mitochondrial eye diseases and secondary mitochondrial changes. Primary mitochondrial eye diseases, for example Leber's hereditary optic atrophy (LHON), retinitis pigmentosa and chronic progressive external ophthalmoplegia are caused by direct damage to mitochondrial function induced by defective genes, either located on mitochondrial DNA (mtDNA) or the DNA of the nucleus (nDNA). In contrast, secondary mitochondrial dysfunctions are caused by environmental factors. In recent years, there has been growing evidence that mitochondrial dysfunctions play an important role in many common eye diseases, such as glaucoma, dry eye, diabetic retinopathy, cataract and age-related macular degeneration (AMD). This article summarises current knowledge of mitochondrial dysfunctions and the role of coenzyme Q10 (CoQ10) as a possible treatment option - with a special focus on glaucoma.

摘要

线粒体功能与眼部健康的诸多方面密切相关。能量产生与活性氧(ROS)生成之间的失衡似乎是线粒体功能障碍发展的原因。由于这种能量不足,眼组织中的氧化应激水平升高,导致多种眼科损伤。区分原发性线粒体眼病和继发性线粒体变化很重要。原发性线粒体眼病,例如Leber遗传性视神经萎缩(LHON)、色素性视网膜炎和慢性进行性外眼肌麻痹,是由位于线粒体DNA(mtDNA)或细胞核DNA(nDNA)上的缺陷基因引起的线粒体功能直接损伤所致。相比之下,继发性线粒体功能障碍是由环境因素引起的。近年来,越来越多的证据表明线粒体功能障碍在许多常见眼病中起重要作用,如青光眼、干眼症、糖尿病视网膜病变、白内障和年龄相关性黄斑变性(AMD)。本文总结了目前关于线粒体功能障碍的知识以及辅酶Q10(CoQ10)作为一种可能的治疗选择的作用——特别关注青光眼。

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