缺血性视神经病变相关分子的病理机制  

Molecular pathologic mechanism associated with ischemic optic neuropathy

作　　者：王晶莹 王影[1] 赵子德[1] 龙思羽 孙婉钰 周芷伊 Jing-Ying Wang;Ying Wang;Zi-De Zhao;Si-Yu Long;Wan-Yu Sun;Zhi-Yi Zhou(Eye Hospital, China Academy of Chinese Medical Sciences, Beijing 100040, China)

机构地区：[1]中国中医科学院眼科医院,中国北京市100040

出　　处：《国际眼科杂志》2021年第7期1187-1190,共4页International Eye Science

基　　金：中国中医科学院基本科研业务费自主选题项目——院内联合创新专项(No.zz11-041)。

摘　　要：非动脉炎性前部缺血性视神经病变(NAION)是由于供应视盘筛板区的睫状后短动脉缺血引起,好发于50岁以上人群,以急性、单眼及无痛性视力下降为特征的急性视神经病变,常导致严重的永久视力损害和视野缺损,日益受到临床科研工作者的重视。本文从NAION发病机制、病理改变,以及既往研究中相关蛋白分子和易感基因方面综述了目前该病的分子病理机制,为今后研究NAION的病理机制及治疗提供理论依据。Nonarteritic anterior ischemic optic neuropathy(NAION)is caused by ischemia of the short posterior ciliary artery that supplies the lamina area of the optic disc.It usually occurs in over 50-year-old people.It is acute optic neuropathy and featured with acute,monocular,and painless vision loss,which frequently results in severe permanent vision damage and visual field defects.This disease is attracting increased attention of clinical researchers.This paper overviews the current molecular pathology of NAION from these aspects,including pathogenesis,pathological changes,relevant protein molecules and susceptibility genes in previous studies.This paper lays a theoretical foundation for future research on the pathological mechanism and the treatment of NAION.

关 键 词：非动脉炎性前部缺血性视神经病变 分子病理机制 蛋白分子 易感基因 

分 类 号：R73[医药卫生—肿瘤]