综述
ENGLISH ABSTRACT
嘌呤能信号在干性年龄相关性黄斑变性中损伤作用的研究进展
胡一凡
孙晓东 [综述]
作者及单位信息
·
DOI: 10.3760/cma.j.cn115989-20190717-00316
Research progress of purinergic signaling in dry age-related macular degeneration
Hu Yifan
Sun Xiaodong
Authors Info & Affiliations
Hu Yifan
Department of Ophthalmology, The General Hospital of Shanghai, Shanghai JiaoTong University, Shanghai 200080, China
Sun Xiaodong
Department of Ophthalmology, The General Hospital of Shanghai, Shanghai JiaoTong University, Shanghai 200080, China
·
DOI: 10.3760/cma.j.cn115989-20190717-00316
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摘要

年龄相关性黄斑变性(AMD)是65岁以上人群重要的致盲眼病,其中干性AMD发病机制复杂,目前仍缺乏有效治疗手段。嘌呤能信号通路广泛存在于视网膜环境中,具有信号传导与神经调节的作用,其可诱导视网膜细胞死亡,调控小胶质细胞活性,参与炎症和氧化应激反应、病理沉积物的生成以及视网膜水肿等病理反应,参与干性AMD的发展过程。本文就嘌呤能信号通路组成分子在RPE、光感受器等多种视网膜细胞的死亡、小胶质细胞的活化调节、病理沉积物的生成以及炎症和氧化应激等多个干性AMD损伤机制的调控中的作用进行综述,以期为临床开展相关研究提供参考。

黄斑变性;嘌呤能受体;综述
ABSTRACT

Age-related macular degeneration (AMD) is one of the major causes of visual loss in people over 65 years of age.There is limited treatment for dry AMD, because of its complex mechanism.Purinergic signaling has the functions of signal transduction and neuro-modulation, participates in the development of dry AMD by regulating retinal cell death, microglial activity, inflammation, pathological deposit formation and retinal edema etc.In this study, we discussed the role and mechanisms involved in dry AMD by introducing the components of the purinergic signaling pathway, and further summarized the regulation of key processes in the pathogenesis of AMD in order to provide a reference for clinical research.

Macular degeneration;Purinergic receptors;Review
Sun Xiaodong, Email: nc.defudabe.utjsnusdx
引用本文

胡一凡,孙晓东. 嘌呤能信号在干性年龄相关性黄斑变性中损伤作用的研究进展[J]. 中华实验眼科杂志,2022,40(01):78-82.

DOI:10.3760/cma.j.cn115989-20190717-00316

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年龄相关性黄斑变性(age-related macular degeneration,AMD)是老年人群中重要的致盲眼病之一 [ 1 ],主要分为干性AMD和湿性AMD。AMD的发病过程中伴随多种病理改变,其中视网膜色素上皮(retinal pigment epithelium,RPE)细胞功能异常和变性是AMD发病早期的关键病理改变之一;光感受器及多种视网膜细胞的死亡是视力下降的直接原因;代谢产物及其他途径来源的物质异常沉积于RPE与Bruch膜之间,形成玻璃膜疣(drusen);RPE与活化的小胶质细胞参与调控的炎症反应既是AMD的病因,也是AMD进展加速的诱因 [ 2 ]。目前湿性AMD可采用抗血管内皮生长因子(vascular endothelial growth factor,VEGF)玻璃体腔注射治疗,但干性AMD发病机制复杂,其仍缺乏有效治愈手段 [ 3 ]
近年研究提示嘌呤能信号通路在干性AMD的发生和发展过程中起着重要作用 [ 4 ]。正常情况下,嘌呤能信号通路参与视网膜多种生理过程 [ 5 ],其中三磷酸腺苷(adenosine triphosphate,ATP)帮助传递光学信号,同时维持视网膜稳态;腺苷通过调控小胶质细胞的活性,影响视网膜免疫炎症反应;ATP和腺苷的表达平衡,为光感受器细胞发挥正常生理功能提供基础;RPE细胞产生的ATP还能促进视网膜神经祖细胞增生。随年龄增加,视网膜环境发生改变,嘌呤能信号通路异常激活导致视网膜多种细胞功能障碍,产生坏死、凋亡、炎症、氧化应激等损伤反应。近年来,嘌呤能信号通路在AMD的多重身份及功能引起了研究者的广泛关注。深入了解嘌呤能信号通路在干性AMD中的作用机制,可以从全新角度解释并补充AMD的发病机制,为更好地治疗干性AMD提供理论依据。
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备注信息
A
孙晓东,Email: nc.defudabe.utjsnusdx
B
所有作者均声明不存在利益冲突
C
国家杰出青年科学基金项目 (81425006)
上海申康医院发展中心临床科技创新项目 (SHDC12016105)
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