眼科

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青光眼发病机制:从临床复杂表型剖析到基本科学问题探索

余晓伟  赵珍妮  杨雪  范志刚   

  1. 中山大学中山眼科中心 眼科学国家重点实验室,广州 510060
  • 收稿日期:2019-11-29 出版日期:2020-01-25 发布日期:2020-02-12
  • 通讯作者: 范志刚,Email: fanzhg3@mail.sysu.edu.cn
  • 基金资助:
    广州市民生科技攻关计划项目(201903010065);中山大学中山眼科中心资助项目(3030902113080)

Pathogenesis of glaucoma: from dissection of complex clinical phenotype to investigation of fundamental scientific problems 

Yu Xiaowei, Zhao Zhenni, Yang Xue, Fan Zhigang. #br#   

  1. State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou 510060, China.
  • Received:2019-11-29 Online:2020-01-25 Published:2020-02-12
  • Contact: Fan Zhigang, Email: fanzhg3@mail.sysu.edu.cn
  • Supported by:
    Guangzhou People's Livelihood Science and Technology Project (201903010065); Zhongshan Eye Center of Sun Yat-sen University Project (3030902113080)

摘要:

青光眼是一类复杂疾病综合征,其共同临床表现为“特征性视神经病变”,实际病因则千差万别。青光眼的发病机制亟待剖析,重点在于梳理其错综复杂的临床表型,围绕眼压改变、视网膜神经节细胞(RGCs)/轴突损伤、非眼压因素等进行合理分型,还原为基础研究手段可以系统探索的基本科学问题。本文将青光眼分为两大类型:I型:真实眼压显著升高,直接导致大量RGCs/轴突原发性损害,并在继发性神经免疫炎症参与下造成青光眼视神经病变(GON)。II型:检测到的眼压不能或者不足以直接导致大量RGCs/轴突损害和GON, 此时神经免疫炎症可能在青光眼的起始发病机制中起到更重要的作用。根据病因机制不同,本文又将前者进一步细分为5型,后者进一步细分为4型。(眼科, 2020, 29: 1-5)

关键词: 青光眼, 视神经病变, 眼压

Abstract: Glaucoma is a complex clinical syndrome with common phenotype of “characteristic optic neuropathy", while its underlying pathogenesis is with multiple etiologies. In order to understand this complex condition, a subclassification strategy based on the characteristics of its clinical phenotype, especially its relationship with intraocular pressure (IOP) elevation, pathophysiology of retinal ganglion cells (RGCs) /their axons and non-IOP mechanism, is imperative. Thereafter, fundamental scientific questions could be raised and investigated using basic research methodology. In this perspective, we have categorized glaucoma into two major sub-categories. Type I: Genuinely elevated IOP to a significant level, which is capable of primarily and directly destroying massive number of RGCs and their axons with subsequent glaucomatous optic neuropathy (GON), while secondary neuroimmune inflammation may participate as an accomplice. Type II: IOP is unable or insufficient to destroy massive RGCs and their axons directly, leading to GON. In this scenario, neuroimmune inflammation may play a more critical role in the initiation and propagation of secondary RGCs/axons damages. Subsequently, we have further subcategorized Type I glaucoma into 5 subtypes and Type II glaucoma into 4 subtypes, respectively. (Ophthalmol CHN, 2020, 29: 1-5)

Key words: glaucoma, optic neuropathy, intraocular pressure