Department of Ophthalmology, King's College Hospital, London SE5 9RS, UK.
Department of Ophthalmology, 417 Veterans Army Hospital (NIMTS), 11521 Athens, Greece.
Cells. 2023 Jul 30;12(15):1969. doi: 10.3390/cells12151969.
This review aims to provide a better understanding of the emerging role of mitophagy in glaucomatous neurodegeneration, which is the primary cause of irreversible blindness worldwide. Increasing evidence from genetic and other experimental studies suggests that mitophagy-related genes are implicated in the pathogenesis of glaucoma in various populations. The association between polymorphisms in these genes and increased risk of glaucoma is presented. Reduction in intraocular pressure (IOP) is currently the only modifiable risk factor for glaucoma, while clinical trials highlight the inadequacy of IOP-lowering therapeutic approaches to prevent sight loss in many glaucoma patients. Mitochondrial dysfunction is thought to increase the susceptibility of retinal ganglion cells (RGCs) to other risk factors and is implicated in glaucomatous degeneration. Mitophagy holds a vital role in mitochondrial quality control processes, and the current review explores the mitophagy-related pathways which may be linked to glaucoma and their therapeutic potential.
本文旨在深入探讨自噬在青光眼神经退行性变中的新作用,因为它是全球范围内导致不可逆失明的主要原因。越来越多的遗传和其他实验研究证据表明,自噬相关基因参与了不同人群的青光眼发病机制。本文还介绍了这些基因的多态性与青光眼风险增加之间的关联。目前,降低眼内压(IOP)是青光眼唯一可改变的危险因素,而临床试验突显了降低 IOP 的治疗方法在许多青光眼患者中预防视力丧失的效果不足。有研究认为,线粒体功能障碍会增加视网膜神经节细胞(RGC)对其他危险因素的易感性,并与青光眼退行性变有关。自噬在维持线粒体质量控制过程中起着至关重要的作用,本文探讨了可能与青光眼有关的自噬相关途径及其治疗潜力。