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Discovery of a normal-tension glaucoma-suspect rhesus macaque with craniocerebral injury:Hints of elevated translaminar cribrosa pressure difference

Discovery of a normal-tension glaucoma-suspect rhesus macaque with craniocerebral injury: Hints of elevated translaminar cribrosa pressure difference

作     者:Jian Wu Qi Zhang Xu Jia Yingting Zhu Zhidong Li Shu Tu Ling Zhao Yifan Du Wei Liu Jiaoyan Ren Liangzhi Xu Hanxiang Yu Fagao Luo Wenru Su Ningli Wang Yehong Zhuo 

作者机构:State Key Laboratory of OphthalmologyZhongshan Ophthalmic CenterGuangdong Provincial Key Laboratory of Ophthalmology and Visual ScienceSun Yat-sen UniversityGuangzhouGuangdong 510060China Beijing Institute of OphthalmologyBeijing Tongren Eye CenterBeijing Tongren HospitalCapital Medical UniversityBeijing Ophthalmology&Visual Sciences Key LaboratoryBeijing 100730China School of Food Sciences and EngineeringSouth China University of TechnologyGuangzhouGuangdong 510641China Guangzhou Huazhen BiosciencesGuangzhouGuangdong 510920China 

出 版 物:《Chinese Medical Journal》 (中华医学杂志(英文版))

年 卷 期:2024年第137卷第4期

页      面:484-486页

核心收录:

学科分类:1002[医学-临床医学] 100212[医学-眼科学] 10[医学] 

基  金:funded by the National Key R&D Project of China(No.2020YFA0112701) National Natural Science Foundation of China(No.82171057) Science and Technology Program of Guangzhou,China(No.202102010216) National Natural Science Foundation of China(No.GZR-2012-009) Beijing Traditional Chinese Medicine Technology Development Fund Project(No.JJ-2018-50) 

主  题:elevated glaucoma diagnosis 

摘      要:To the Editor:Normal-tension glaucoma(NTG)is a progressive optic neuropathy characterized by irreversible blindness with statistically normal intraocular pressure(IOP)(≤21 mmHg),^([1,2])which makes early-stage diagnosis in the clinical practice difficult.Pathophysiological pathways underlying NTG include vascular dysregulation,toxic metabolite accumulation,and elevated translaminar cribrosa pressure difference(TLCPD).^([3])Although various small animal models have provided evidence of different pathophysiological mechanisms,the complicated clinical phenotype cannot be fully imitated by secondary disease models,and the gap between rodents and humans weakens their translational potential.Thus,the pathological changes associated with NTG remain unclear.

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