[1]张梦圆,魏婷婷,谢田华,等.Rac1介导的氧化应激在糖尿病视网膜病变中的作用[J].眼科新进展,2020,40(12):1185-1187.[doi:10.13389/j.cnki.rao.2020.0263]
 ZHANG Mengyuan,WEI Tingting,XIE Tianhua,et al.Role of Rac1-mediated oxidative stress in diabetic retinopathy[J].Recent Advances in Ophthalmology,2020,40(12):1185-1187.[doi:10.13389/j.cnki.rao.2020.0263]
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Rac1介导的氧化应激在糖尿病视网膜病变中的作用/HTML
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《眼科新进展》[ISSN:1003-5141/CN:41-1105/R]

卷:
40卷
期数:
2020年12期
页码:
1185-1187
栏目:
文献综述
出版日期:
2020-12-05

文章信息/Info

Title:
Role of Rac1-mediated oxidative stress in diabetic retinopathy
文章编号:
1185
作者:
张梦圆魏婷婷谢田华姚勇
214023 江苏省无锡市,南京医科大学附属无锡人民医院眼科
Author(s):
ZHANG MengyuanWEI TingtingXIE TianhuaYAO Yong
Department of Ophthalmology,Wuxi People’s Hospital Affiliated to Nanjing Medical University,Wuxi 214023,Jiangsu Province,China
关键词:
Rac1Nox2氧化应激糖尿病视网膜病变
Keywords:
Rac1 Nox2 oxidative stressdiabetic retinopathy
分类号:
R774.1
DOI:
10.13389/j.cnki.rao.2020.0263
文献标志码:
A
摘要:
糖尿病视网膜病变(diabetic retinopathy,DR)是高龄人群主要致盲原因之一。进一步探寻DR预防、治疗方向具有重要意义。Rac1/Nox2通路参与细胞黏附、凋亡及细胞骨架重组调控,在细胞信号转导中发挥重要作用。越来越多的研究表明,激活Rac1/Nox2通路可显著促进DR发生发展,提示调控Rac1/Nox2通路是DR潜在治疗方向。本文主要阐述了Rac1在DR中的作用,旨在为DR相关研究提供可靠方向。
Abstract:
Diabetic retinopathy (DR) is the major vision-threatening eye disease in theworking-age population. The search for new therapies with fewer side effects and better effectiveness is of great significance. Rac1/Nox2 pathway is involved in the regulation of cell adhesion, proliferation, apoptosis and cytoskeletal recombination, and plays an important role in signal transduction and communication between cells. More and more studies have shown that Rac1/Nox2 pathway plays a role in the pathogenesis of diabetic retinopathy, which suggests that Rac1/Nox2 pathway might be considered as a potential therapeutic approach for the treatment of DR. This review mainly elaboratesnew insights into the role of Rac1 in the development of diabetic retinopathy and provides thereliable direction for thetreatment of diabetic retinopathy.

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备注/Memo

备注/Memo:
国家自然科学基金面上项目(编号:81770941);江苏省科教强卫重点学科项目(编号:ZDXKC2016008)
更新日期/Last Update: 2020-12-05