青光眼视神经病变:视网膜神经节细胞的线粒体动力学、功能障碍和保护

IF 18.6 1区 医学 Q1 OPHTHALMOLOGY
Won-Kyu Ju , Guy A. Perkins , Keun-Young Kim , Tonking Bastola , Woo-Young Choi , Soo-Ho Choi
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引用次数: 14

摘要

青光眼是世界范围内不可逆失明的主要原因,其特点是视网膜神经节细胞(RGCs)及其轴突的缓慢、进行性和多因素变性,导致视力丧失。尽管青光眼在60岁及以上人群中发病率很高,但导致青光眼进展的因素目前还没有很好的特征。眼压(IOP)是唯一被证实可治疗的危险因素。然而,降低眼压不足以预防疾病进展。青光眼发病机制的一个重要研究方向是了解RGCs及其轴突和突触中线粒体的结构和功能损伤。青光眼的危险因素,如眼压升高、衰老、遗传变异、神经炎症、神经营养因子剥夺和血管失调,都是青光眼线粒体功能障碍的潜在诱发因素。由于氧化磷酸化应激介导的线粒体功能障碍与青光眼RGCs线粒体结构和功能损伤有关,了解线粒体结构和功能改变的潜在机制及其关系将有助于在青光眼RGCs及其轴突和突触中开发线粒体相关的神经保护作用,以对抗青光眼神经变性。在这里,我们回顾了目前关于青光眼RGCs线粒体动力学基础结构和功能改变的研究,以及保护RGCs免受青光眼神经变性的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Glaucomatous optic neuropathy: Mitochondrial dynamics, dysfunction and protection in retinal ganglion cells

Glaucoma is a leading cause of irreversible blindness worldwide and is characterized by a slow, progressive, and multifactorial degeneration of retinal ganglion cells (RGCs) and their axons, resulting in vision loss. Despite its high prevalence in individuals 60 years of age and older, the causing factors contributing to glaucoma progression are currently not well characterized. Intraocular pressure (IOP) is the only proven treatable risk factor. However, lowering IOP is insufficient for preventing disease progression. One of the significant interests in glaucoma pathogenesis is understanding the structural and functional impairment of mitochondria in RGCs and their axons and synapses. Glaucomatous risk factors such as IOP elevation, aging, genetic variation, neuroinflammation, neurotrophic factor deprivation, and vascular dysregulation, are potential inducers for mitochondrial dysfunction in glaucoma. Because oxidative phosphorylation stress-mediated mitochondrial dysfunction is associated with structural and functional impairment of mitochondria in glaucomatous RGCs, understanding the underlying mechanisms and relationship between structural and functional alterations in mitochondria would be beneficial to developing mitochondria-related neuroprotection in RGCs and their axons and synapses against glaucomatous neurodegeneration. Here, we review the current studies focusing on mitochondrial dynamics-based structural and functional alterations in the mitochondria of glaucomatous RGCs and therapeutic strategies to protect RGCs against glaucomatous neurodegeneration.

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来源期刊
CiteScore
34.10
自引率
5.10%
发文量
78
期刊介绍: Progress in Retinal and Eye Research is a Reviews-only journal. By invitation, leading experts write on basic and clinical aspects of the eye in a style appealing to molecular biologists, neuroscientists and physiologists, as well as to vision researchers and ophthalmologists. The journal covers all aspects of eye research, including topics pertaining to the retina and pigment epithelial layer, cornea, tears, lacrimal glands, aqueous humour, iris, ciliary body, trabeculum, lens, vitreous humour and diseases such as dry-eye, inflammation, keratoconus, corneal dystrophy, glaucoma and cataract.
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