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原发性开角型青光眼的生物标志物

Biomarkers of primary open-angle glaucoma.

作者信息

Knepper Paul A, Samples John R, Yue Beatrice Yjt

机构信息

Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, 1855 West Taylor, Chicago, IL 60612, USA ; Department of Ophthalmology, Northwestern University Medical School, 150 East Huron, Suite 1000, Chicago, IL 60611, USA.

Casey Eye Institute, Oregon Health and Sciences University, Portland, OR, USA ; Rocky Vista University, 11960 Lioness Way, Parker, CO 80134, USA.

出版信息

Expert Rev Ophthalmol. 2010 Dec;5(6):731-742. doi: 10.1586/EOP.10.73.

DOI:10.1586/EOP.10.73
PMID:26435732
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4590996/
Abstract

Primary open-angle glaucoma (POAG) is a primary neuronal disease of the optic nerve without a definable cause, and is often associated with increased intraocular pressure. Worldwide, POAG is the second leading cause of blindness; there are 45 million people today with POAG and bilateral blindness is present in 4.5 million of these. In order to elucidate the possible etiologic factors in POAG, we have cataloged all known biomarkers in the aqueous humor, trabecular meshwork, optic nerve and blood into four categories, namely extracellular matrix (ECM), cell signaling molecules, aging/stress and immunity-related changes. We present a theoretical model to show possible signaling pathways of the ECM, cell signaling and innate immune response through activation of Toll-like receptor 4. Our article suggests that ECM and innate immune biomarkers are the lead candidates for developing the 'POAG biomarker signature'. We suggest that current research is critical to pinpoint the causes of the disease so that new treatment modalities can become available for better regulation of the intraocular pressure and neuroprotection of the optic nerve.

摘要

原发性开角型青光眼(POAG)是一种病因不明的原发性视神经疾病,常与眼压升高有关。在全球范围内,POAG是导致失明的第二大主要原因;目前有4500万人患有POAG,其中450万人双眼失明。为了阐明POAG可能的病因,我们已将房水、小梁网、视神经和血液中所有已知的生物标志物归类为四类,即细胞外基质(ECM)、细胞信号分子、衰老/应激和免疫相关变化。我们提出了一个理论模型,以展示通过激活Toll样受体4,ECM、细胞信号和先天免疫反应可能的信号通路。我们的文章表明,ECM和先天免疫生物标志物是开发“POAG生物标志物特征”的主要候选物。我们认为,当前的研究对于查明该疾病的病因至关重要,以便能够采用新的治疗方法更好地调节眼压并对视神经进行神经保护。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2657/4590996/dcde34508bc4/nihms264171f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2657/4590996/b14f2ee56250/nihms264171f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2657/4590996/dcde34508bc4/nihms264171f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2657/4590996/b14f2ee56250/nihms264171f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2657/4590996/dcde34508bc4/nihms264171f2.jpg

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本文引用的文献

1
Common variants near CAV1 and CAV2 are associated with primary open-angle glaucoma.CAV1 和 CAV2 附近的常见变异与原发性开角型青光眼有关。
Nat Genet. 2010 Oct;42(10):906-9. doi: 10.1038/ng.661. Epub 2010 Sep 12.
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Diagnosis-independent Alzheimer disease biomarker signature in cognitively normal elderly people.认知正常老年人中与诊断无关的阿尔茨海默病生物标志物特征
Arch Neurol. 2010 Aug;67(8):949-56. doi: 10.1001/archneurol.2010.179.
3
Detection of Alzheimer peptides and chemokines in the aqueous humor.房水中阿尔茨海默肽和趋化因子的检测。
神经保护能否有效治疗原发性开角型青光眼?一项系统评价与荟萃分析方案。
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4
BMP and Activin Membrane Bound Inhibitor Regulates the Extracellular Matrix in the Trabecular Meshwork.BMP 和激活素的细胞膜结合抑制剂调节小梁网细胞外基质。
Invest Ophthalmol Vis Sci. 2018 Apr 1;59(5):2154-2166. doi: 10.1167/iovs.17-23282.
5
Strategies to Reduce Oxidative Stress in Glaucoma Patients.青光眼患者氧化应激的缓解策略。
Curr Neuropharmacol. 2018;16(7):903-918. doi: 10.2174/1570159X15666170705101910.
6
TGF-β induces phosphorylation of phosphatase and tensin homolog: implications for fibrosis of the trabecular meshwork tissue in glaucoma.TGF-β 诱导磷酸酶和张力蛋白同源物的磷酸化:对青光眼小梁网组织纤维化的影响。
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7
ABCB1 transporter and Toll-like receptor 4 in trabecular meshwork cells.小梁网细胞中的ABCB1转运蛋白和Toll样受体4
Mol Vis. 2015 Mar 5;21:201-12. eCollection 2015.
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sCD44 overexpression increases intraocular pressure and aqueous outflow resistance.可溶性CD44过表达会增加眼压和房水流出阻力。
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The Human Eye Proteome Project: perspectives on an emerging proteome.人类眼睛蛋白质组计划:新兴蛋白质组学的展望。
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