Centre for Eye Research Australia, Department of Ophthalmology, University of Melbourne, Royal Victorian Eye and Ear Hospital, East Melbourne, Vic., Australia.
Ophthalmic Res. 2010;44(3):173-8. doi: 10.1159/000316478. Epub 2010 Sep 9.
Aging is the greatest risk factor for glaucoma, implying that intrinsic age-related changes to retinal ganglion cells, their supporting tissue or both make retinal ganglion cells susceptible to injury. Changes to the ocular vasculature, connective tissue of the optic nerve head and mitochondria, which have been documented with advancing age and shown to be exacerbated in glaucoma, may predispose to glaucomatous injury. When considering such age-related changes, it is difficult to separate pathological change from physiological change, and cause from consequence. The insults that predispose aged retinal ganglion cells to injury are likely to be varied and multiple; therefore, it may be more relevant to identify and treat common mechanisms that predispose to retinal ganglion cell failure and/or death. We suggest that mitochondrial dysfunction, as either a cause or consequence of injury, renders retinal ganglion cells sensitive to degeneration. Therapeutic approaches that target mitochondria and promote energy production may provide a general means of protecting aged retinal ganglion cells from degeneration, regardless of the etiology.
衰老是青光眼的最大风险因素，这意味着视网膜神经节细胞及其支持组织或两者的内在年龄相关变化使视网膜神经节细胞容易受到损伤。随着年龄的增长而发生的眼部血管、视神经头部结缔组织和线粒体的变化，以及在青光眼患者中加剧的变化，可能会导致青光眼损伤。在考虑这些与年龄相关的变化时，很难将病理性改变与生理性改变以及病因与后果区分开来。使衰老的视网膜神经节细胞容易受到损伤的损伤可能是多种多样的；因此，识别和治疗易导致视网膜神经节细胞衰竭和/或死亡的常见机制可能更为相关。我们认为，线粒体功能障碍无论是损伤的原因还是结果，都会使视网膜神经节细胞容易发生变性。针对线粒体并促进能量产生的治疗方法可能为保护衰老的视网膜神经节细胞免受变性提供一种通用手段，而与病因无关。
