• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

血视网膜屏障中的关键紧密连接蛋白。

Key Claudins at the Blood-Retina Barriers.

作者信息

Hashimoto Yosuke, Campbell Matthew

机构信息

Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.

Smurfit Institute of Genetics, Trinity College Dublin, Dublin, Ireland.

出版信息

Adv Exp Med Biol. 2025;1468:447-451. doi: 10.1007/978-3-031-76550-6_73.

DOI:10.1007/978-3-031-76550-6_73
PMID:39930236
Abstract

Tight junctions are physical barriers that limit the paracellular diffusion of solutes and ions. The blood-retina barriers are cellular barriers composed of tight junctions established in retinal pigment epithelial (RPE) cells and retinal endothelial cells to maintain retinal homeostasis. Claudins are the major components of tight junctions, and their dysregulation leads to impaired blood-retina barrier integrity, resulting in retinal diseases with concomitant local inflammation. In this chapter, we introduce two important claudins, claudin-5 and -19, and briefly explain how decreased expression of these claudins is associated with the progress of diabetic retinopathy (DR) and age-related macular degeneration (AMD) by compromising the blood-retina barriers.

摘要

紧密连接是限制溶质和离子细胞旁扩散的物理屏障。血视网膜屏障是由视网膜色素上皮(RPE)细胞和视网膜内皮细胞中建立的紧密连接组成的细胞屏障,以维持视网膜内环境稳定。闭合蛋白是紧密连接的主要成分,其失调会导致血视网膜屏障完整性受损,从而引发伴有局部炎症的视网膜疾病。在本章中,我们介绍两种重要的闭合蛋白,即闭合蛋白-5和-19,并简要解释这些闭合蛋白的表达降低如何通过损害血视网膜屏障而与糖尿病视网膜病变(DR)和年龄相关性黄斑变性(AMD)的进展相关。

相似文献

1
Key Claudins at the Blood-Retina Barriers.血视网膜屏障中的关键紧密连接蛋白。
Adv Exp Med Biol. 2025;1468:447-451. doi: 10.1007/978-3-031-76550-6_73.
2
Integration of tight junctions and claudins with the barrier functions of the retinal pigment epithelium.紧密连接和 Claudin 与视网膜色素上皮的屏障功能整合。
Prog Retin Eye Res. 2011 Sep;30(5):296-323. doi: 10.1016/j.preteyeres.2011.06.002. Epub 2011 Jun 17.
3
Claudin-3 and claudin-19 partially restore native phenotype to ARPE-19 cells via effects on tight junctions and gene expression.Claudin-3和Claudin-19通过影响紧密连接和基因表达,部分恢复了ARPE-19细胞的天然表型。
Exp Eye Res. 2016 Oct;151:179-89. doi: 10.1016/j.exer.2016.08.021. Epub 2016 Sep 1.
4
The effect of claudin-5 overexpression on the interactions of claudin-1 and -2 and barrier function in retinal cells.紧密连接蛋白5过表达对视网膜细胞中紧密连接蛋白1和2的相互作用及屏障功能的影响。
Curr Mol Med. 2014;14(9):1226-37. doi: 10.2174/1566524014666141015160355.
5
Vascular endothelial growth factor-Ab ameliorates outer-retinal barrier and vascular dysfunction in the diabetic retina.血管内皮生长因子-Ab可改善糖尿病视网膜病变中外侧视网膜屏障及血管功能障碍。
Clin Sci (Lond). 2017 Jun 1;131(12):1225-1243. doi: 10.1042/CS20170102. Epub 2017 Mar 24.
6
Claudins regulate gene and protein expression of the retinal pigment epithelium independent of their association with tight junctions.紧密连接蛋白通过调节基因和蛋白表达影响视网膜色素上皮细胞的功能。
Exp Eye Res. 2020 Sep;198:108157. doi: 10.1016/j.exer.2020.108157. Epub 2020 Jul 23.
7
The blood-retina barrier: tight junctions and barrier modulation.血视网膜屏障:紧密连接和屏障调节。
Adv Exp Med Biol. 2012;763:70-84.
8
Oxidized low density lipoprotein-induced senescence of retinal pigment epithelial cells is followed by outer blood-retinal barrier dysfunction.氧化型低密度脂蛋白诱导的视网膜色素上皮细胞衰老继而导致外血-视网膜屏障功能障碍。
Int J Biochem Cell Biol. 2012 May;44(5):808-14. doi: 10.1016/j.biocel.2012.02.005. Epub 2012 Feb 13.
9
Intracellular amyloid beta alters the tight junction of retinal pigment epithelium in 5XFAD mice.细胞内淀粉样蛋白β改变5XFAD小鼠视网膜色素上皮的紧密连接。
Neurobiol Aging. 2014 Sep;35(9):2013-20. doi: 10.1016/j.neurobiolaging.2014.03.008. Epub 2014 Mar 15.
10
Oxidative stress-mediated TXNIP loss causes RPE dysfunction.氧化应激介导的 TXNIP 缺失导致 RPE 功能障碍。
Exp Mol Med. 2019 Oct 15;51(10):1-13. doi: 10.1038/s12276-019-0327-y.

本文引用的文献

1
Claudin-1 interacts with EPHA2 to promote cancer stemness and chemoresistance in colorectal cancer.Claudin-1 与 EPHA2 相互作用,促进结直肠癌中的癌症干细胞特性和化疗耐药性。
Cancer Lett. 2023 Nov 28;579:216479. doi: 10.1016/j.canlet.2023.216479. Epub 2023 Nov 2.
2
The CLDN5 gene at the blood-brain barrier in health and disease.血脑屏障中 CLDN5 基因在健康和疾病中的作用。
Fluids Barriers CNS. 2023 Mar 28;20(1):22. doi: 10.1186/s12987-023-00424-5.
3
Cholesterol-rich domain formation mediated by ZO proteins is essential for tight junction formation.
由 ZO 蛋白介导的富含胆固醇的域形成对于紧密连接的形成是必需的。
Proc Natl Acad Sci U S A. 2023 Feb 21;120(8):e2217561120. doi: 10.1073/pnas.2217561120. Epub 2023 Feb 15.
4
Variants in CLDN5 cause a syndrome characterized by seizures, microcephaly and brain calcifications.CLDN5 变异导致一种以癫痫发作、小头畸形和脑钙化为特征的综合征。
Brain. 2023 Jun 1;146(6):2285-2297. doi: 10.1093/brain/awac461.
5
Nanoscale segregation of channel and barrier claudins enables paracellular ion flux.纳米尺度上的通道和屏障紧密连接蛋白的分隔使细胞旁离子通量成为可能。
Nat Commun. 2022 Aug 25;13(1):4985. doi: 10.1038/s41467-022-32533-4.
6
Tight junction formation by a claudin mutant lacking the COOH-terminal PDZ domain-binding motif.紧密连接形成由缺乏羧基末端 PDZ 结构域结合基序的 Claudin 突变体。
Ann N Y Acad Sci. 2022 Oct;1516(1):85-94. doi: 10.1111/nyas.14881. Epub 2022 Aug 9.
7
Recurrent de novo mutations in CLDN5 induce an anion-selective blood-brain barrier and alternating hemiplegia.CLDN5 中的反复新生突变导致阴离子选择性血脑屏障和交替性偏瘫。
Brain. 2022 Oct 21;145(10):3374-3382. doi: 10.1093/brain/awac215.
8
Loss of CLDN5 in podocytes deregulates WIF1 to activate WNT signaling and contributes to kidney disease.足细胞中 Claudin5 的缺失会使 WIF1 失活,从而激活 WNT 信号通路,并导致肾脏疾病。
Nat Commun. 2022 Mar 24;13(1):1600. doi: 10.1038/s41467-022-29277-6.
9
An inducible Cldn11-CreER mouse line for selective targeting of lymphatic valves.诱导型 Claudin11-CreER 小鼠品系用于选择性靶向淋巴管瓣膜。
Genesis. 2021 Aug;59(7-8):e23439. doi: 10.1002/dvg.23439. Epub 2021 Aug 2.
10
Acute mechanical stress in primary porcine RPE cells induces angiogenic factor expression and in vitro angiogenesis.原代猪视网膜色素上皮细胞中的急性机械应力诱导血管生成因子表达及体外血管生成。
J Biol Eng. 2020 Apr 25;14:13. doi: 10.1186/s13036-020-00235-4. eCollection 2020.