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作 者:钟勇 卢玥竹 Zhong Yong;Lu Yuezhu(Department of Ophthalmology,Peking Union Medical College Hospital,Key Laboratory of Ocular Fundus Diseases,Chinese Academy of Medical Science,Beijing 100730,China)
机构地区:[1]中国医学科学院北京协和医院眼科、中国医学科学院眼底重点实验室,北京100730
出 处:《中华眼底病杂志》2023年第11期883-886,共4页Chinese Journal of Ocular Fundus Diseases
基 金:中央高水平医院临床科研项目(2022-PUMCH-B-103)。
摘 要:视网膜神经节细胞(RGC)的原发性或继发性死亡是临床中多种视神经疾病的共同转归,常导致严重的视功能损害。RGC的内在特点是在细胞分化成熟过程中,细胞内在的生长抑制因子转录因子不断上调,生长诱导转录因子不断下调。同时,RGC受损后外在的抑制性微环境包括氧化应激、慢性炎症、神经营养因子缺乏、髓鞘蛋白的高度表达和胶质瘢痕的形成均限制了轴突的再生。内在和外在因素共同导致受损后RGC的死亡并阻碍轴突再生。多种神经保护制剂及方法试图从内在和外在两方面促进神经保护及轴突再生,熟知这些神经保护策略对进一步拓展该领域的基础研究及推动其向临床转化有着重要意义。Primary or secondary death of retinal ganglion cells(RGC)is a common outcome in various optic neuropathies,often resulting in severe visual damage.The inherent characteristics of RGC include the continuous upregulation of intracellular growth-inhibitory transcription factors and the downregulation of growth-inducing transcription factors during cell differentiation.Additionally,the external inhibitory microenvironment following RGC damage,including oxidative stress,chronic inflammation,lack of neurotrophic factors,high expression of myelin proteins,and the formation of glial scars,all restrict axonal regeneration.Both intrinsic and extrinsic factors lead to the death of damaged RGC and hinder axonal regeneration.Various neuroprotective agents and methods attempt to promote neuroprotection and axonal regeneration from both intrinsic and extrinsic aspects,and well knowledge of these neuroprotective strategies is of significant importance for promoting the neuroprotective experimental research and facilitating its translation into clinical practice.
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