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本文引用的文献

1
Autophagy in the eye: Development, degeneration, and aging.眼内自噬:发育、变性和衰老。
Prog Retin Eye Res. 2016 Nov;55:206-245. doi: 10.1016/j.preteyeres.2016.08.001. Epub 2016 Aug 23.
2
Autophagy and Mitochondrial Dysfunction in Tenon Fibroblasts from Exfoliation Glaucoma Patients.剥脱性青光眼患者Tenon成纤维细胞中的自噬与线粒体功能障碍
PLoS One. 2016 Jul 8;11(7):e0157404. doi: 10.1371/journal.pone.0157404. eCollection 2016.
3
Autophagy and mechanotransduction in outflow pathway cells.房水流出通路细胞中的自噬与机械转导
Exp Eye Res. 2017 May;158:146-153. doi: 10.1016/j.exer.2016.06.021. Epub 2016 Jun 29.
4
Unconventional secretion of misfolded proteins promotes adaptation to proteasome dysfunction in mammalian cells.错误折叠蛋白的非常规分泌促进哺乳动物细胞对蛋白酶体功能障碍的适应。
Nat Cell Biol. 2016 Jul;18(7):765-76. doi: 10.1038/ncb3372. Epub 2016 Jun 13.
5
Evaluation of Lamina Cribrosa and Choroid in Nonglaucomatous Patients With Pseudoexfoliation Syndrome Using Spectral-Domain Optical Coherence Tomography.使用频域光学相干断层扫描技术评估假性剥脱综合征非青光眼患者的筛板和脉络膜
Invest Ophthalmol Vis Sci. 2016 Mar;57(3):1293-300. doi: 10.1167/iovs.15-18312.
6
Systemic Associations of Exfoliation Syndrome.剥脱综合征的全身关联
Asia Pac J Ophthalmol (Phila). 2016 Jan-Feb;5(1):45-50. doi: 10.1097/APO.0000000000000187.
7
Ethnicity-Based Differences in the Association of LOXL1 Polymorphisms with Pseudoexfoliation/Pseudoexfoliative Glaucoma: A Meta-Analysis.赖氨酰氧化酶样蛋白1(LOXL1)基因多态性与假性剥脱综合征/假性剥脱性青光眼相关性的种族差异:一项荟萃分析
Ann Hum Genet. 2015 Nov;79(6):431-50. doi: 10.1111/ahg.12128. Epub 2015 Sep 24.
8
Genetic variants and cellular stressors associated with exfoliation syndrome modulate promoter activity of a lncRNA within the LOXL1 locus.与剥脱综合征相关的基因变异和细胞应激源可调节LOXL1基因座内一个长链非编码RNA的启动子活性。
Hum Mol Genet. 2015 Nov 15;24(22):6552-63. doi: 10.1093/hmg/ddv347. Epub 2015 Aug 25.
9
A common variant mapping to CACNA1A is associated with susceptibility to exfoliation syndrome.一个定位到CACNA1A基因的常见变异与剥脱综合征易感性相关。
Nat Genet. 2015 Apr;47(4):387-92. doi: 10.1038/ng.3226. Epub 2015 Feb 23.
10
Update on pseudoexfoliation syndrome pathogenesis and associations with intraocular pressure, glaucoma and systemic diseases.假性剥脱综合征的发病机制及其与眼压、青光眼和全身性疾病的关联的最新进展
Curr Opin Ophthalmol. 2015 Mar;26(2):82-9. doi: 10.1097/ICU.0000000000000132.

自噬功能障碍是剥脱性青光眼的关键吗?

Is Autophagy Dysfunction a Key to Exfoliation Glaucoma?

机构信息

Departments of Ophthalmology.

Einhorn Clinical Research Center, New York Eye and Ear Infirmary of Mount Sinai, New York, NY.

出版信息

J Glaucoma. 2018 Mar;27(3):197-201. doi: 10.1097/IJG.0000000000000606.

DOI:10.1097/IJG.0000000000000606
PMID:27977481
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5468508/
Abstract

In this short report we review previous work toward the identification of the protein and cellular sources of exfoliation glaucoma and described our recent finding on dysfunction of autophagy in Tenon capsule fibroblasts obtained from exfoliation syndrome glaucoma patients at the time of surgery and discuss the potential implications of these findings for understanding the cellular sources of the disease.

摘要

在这份简短的报告中,我们回顾了之前针对剥脱性青光眼的蛋白质和细胞来源的鉴定工作,并描述了我们最近在手术时从剥脱综合征青光眼患者的眼外囊组织中获得的成纤维细胞中的自噬功能障碍方面的发现,并讨论了这些发现对理解疾病的细胞来源的潜在意义。