Neuroprotection in glaucoma： present and future

• Published in: Chinese medical journal Vol. 126; no. 8; pp. 1567 - 1577
• Main Authors: Chen, Shi-da, Wang, Lu, Zhang, Xiu-lan
• Format: Journal Article
• Language: English
• Published: China Zhongshan Ophthalmic Center, State Key Laboratory of Ophthalmology, Sun Yat-sen University, Guangzhou, Guangdong 510060, China 2013
• Subjects: Apoptosis; Axonal Transport; Brain-Derived Neurotrophic Factor - physiology; Ciliary Neurotrophic Factor - physiology; Glaucoma - etiology; Glaucoma - therapy; Humans; Mitochondria - physiology; Neuroprotective Agents - therapeutic use; Oxidative Stress; Protein Folding; PubMed; Receptors, N-Methyl-D-Aspartate - physiology; Retinal Ganglion Cells - physiology; 保护策略; 功能障碍; 搜索策略; 神经保护作用; 神经营养因子; 视网膜神经节细胞; 青光眼; glaucoma; neuroprotection; retinal ganglion cells
• ISSN: 0366-6999; 2542-5641
• DOI: 10.3760/cma.j.issn.0366-6999.20123565

Objective To review the updated research on neuroprotection in glaucoma, and summarize the potential agents investigated so far. Data sources The data in this review were collected from PubMed and Google Scholar databases published in English up to September 2012, with keywords including glaucoma, neuroprotection, and retinal ganglion cells, both alone and in combination. Publications from the past ten years were selected, but important older articles were not excluded. Study selection Articles about neuroprotection in glaucoma were selected and reviewed, and those that are cited in articles identified by this search strategy and judged relevant to this review were also included. Results Although lowering the intraocular pressure is the only therapy approved as being effective in the treatment of glaucoma, increasing numbers of studies have discovered various mechanisms of retinal ganglion cells death in the glaucoma and relevant neuroprotective strategies. These strategies target neurotrophic factor deprivation, excitotoxic damage, oxidative stress, mitochondrial dysfunction, inflammation, activation of intrinsic and extrinsic apoptotic signals, ischemia, and protein misfolding. Exploring the mechanism of axonal transport failure, synaptic dysfunction, the glial system in glaucoma, and stem cell used in glaucoma constitute promising research areas of the future. Conclusions Neuroprotective strategies continue to be refined, and future deep investment in researching the pathogenesis of glaucoma may provide novel and practical neuroprotection tactics. Establishing a system to assess the effects of neuroprotection treatments may further facilitate this research.