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本文引用的文献

1
Adiponectin, Insulin Sensitivity and Diabetic Retinopathy in Latinos With Type 2 Diabetes.2型糖尿病拉丁裔人群中的脂联素、胰岛素敏感性与糖尿病视网膜病变
J Clin Endocrinol Metab. 2015 Sep;100(9):3348-55. doi: 10.1210/jc.2015-1221. Epub 2015 May 28.
2
Immune complex formation in human diabetic retina enhances toxicity of oxidized LDL towards retinal capillary pericytes.人类糖尿病视网膜中的免疫复合物形成增强了氧化型低密度脂蛋白对视网膜毛细血管周细胞的毒性。
J Lipid Res. 2014 May;55(5):860-9. doi: 10.1194/jlr.M045401. Epub 2014 Mar 10.
3
Posttranslational modification of mitochondrial transcription factor A in impaired mitochondria biogenesis: implications in diabetic retinopathy and metabolic memory phenomenon.线粒体转录因子 A 在受损线粒体生物发生中的翻译后修饰:在糖尿病性视网膜病变和代谢记忆现象中的意义。
Exp Eye Res. 2014 Apr;121:168-77. doi: 10.1016/j.exer.2014.02.010. Epub 2014 Mar 4.
4
Pathophysiology of diabetic retinopathy.糖尿病视网膜病变的病理生理学
ISRN Ophthalmol. 2013 Jan 15;2013:343560. doi: 10.1155/2013/343560. eCollection 2013.
5
TIAM1-RAC1 signalling axis-mediated activation of NADPH oxidase-2 initiates mitochondrial damage in the development of diabetic retinopathy.TIAM1-RAC1信号轴介导的NADPH氧化酶-2激活在糖尿病视网膜病变发展过程中引发线粒体损伤。
Diabetologia. 2014 May;57(5):1047-56. doi: 10.1007/s00125-014-3194-z. Epub 2014 Feb 20.
6
The role of O-GlcNAc signaling in the pathogenesis of diabetic retinopathy.O-GlcNAc 信号通路在糖尿病视网膜病变发病机制中的作用。
Proteomics Clin Appl. 2014 Apr;8(3-4):218-31. doi: 10.1002/prca.201300076. Epub 2014 Feb 19.
7
Replication of genetic loci implicated in diabetic retinopathy.遗传位点在糖尿病视网膜病变中的复制。
Invest Ophthalmol Vis Sci. 2014 Mar 19;55(3):1666-71. doi: 10.1167/iovs.13-13559.
8
Prevalence and risk factors for diabetic retinopathy in Asian Indians with young onset type 1 and type 2 diabetes.亚洲印度裔早发型1型和2型糖尿病患者糖尿病视网膜病变的患病率及危险因素
J Diabetes Complications. 2014 May-Jun;28(3):291-7. doi: 10.1016/j.jdiacomp.2013.12.008. Epub 2014 Jan 6.
9
Beneficial effects of the nutritional supplements on the development of diabetic retinopathy.营养补充剂对糖尿病视网膜病变发展的有益影响。
Nutr Metab (Lond). 2014 Jan 30;11(1):8. doi: 10.1186/1743-7075-11-8.
10
Antioxidant drug therapy approaches for neuroprotection in chronic diseases of the retina.用于视网膜慢性疾病神经保护的抗氧化药物治疗方法。
Int J Mol Sci. 2014 Jan 27;15(2):1865-86. doi: 10.3390/ijms15021865.

氧化应激诱导糖尿病视网膜病变发生发展的相关机制。

Mechanisms involved in the development of diabetic retinopathy induced by oxidative stress.

作者信息

Guzman David Calderón, Olguín Hugo Juárez, García Ernestina Hernández, Peraza Armando Valenzuela, de la Cruz Diego Zamora, Soto Monica Punzo

机构信息

a Laboratory of Neurochemistry , National Institute of Pediatrics , Mexico.

b Laboratory of Pharmacology , National Institute of Pediatrics , Mexico.

出版信息

Redox Rep. 2017 Jan;22(1):10-16. doi: 10.1080/13510002.2016.1205303. Epub 2016 Jul 15.

DOI:10.1080/13510002.2016.1205303
PMID:27420399
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6837689/
Abstract

BACKGROUND

Diabetic retinopathy (DR) is one of the main complications in patients with diabetes and has been the leading cause of visual loss since 1990. Oxidative stress is a biological process resulting from excessive production of reactive oxygen species (ROS). This process contributes to the development of many diseases and disease complications. ROS interact with various cellular components to induce cell injury. Fortunately, there is an antioxidan t system that protects organisms against ROS. Indeed, when ROS exceed antioxidant capacity, the resulting cell injury can cause diverse physiological and pathological changes that could lead to a disease like DR.

OBJECTIVE

This paper reviews the possible mechanisms of common and novel biomarkers involved in the development of DR and explores how these biomarkers could be used to monitor the damage induced by oxidative stress in DR, which is a significant complication in people with diabetes.

CONCLUSION

The poor control of glucemy in pacients with DB has been shown contribute to the development of complications in eyes as DR.

摘要

背景

糖尿病视网膜病变(DR)是糖尿病患者的主要并发症之一,自1990年以来一直是视力丧失的主要原因。氧化应激是一种由活性氧(ROS)过量产生导致的生物学过程。这一过程促使许多疾病及其并发症的发展。ROS与各种细胞成分相互作用以诱导细胞损伤。幸运的是,存在一个抗氧化系统来保护生物体免受ROS的侵害。实际上,当ROS超过抗氧化能力时,由此产生的细胞损伤会导致各种生理和病理变化,进而可能引发像DR这样的疾病。

目的

本文综述了参与DR发生发展的常见和新型生物标志物的可能机制,并探讨这些生物标志物如何用于监测糖尿病患者这一重大并发症DR中氧化应激诱导的损伤。

结论

已表明糖尿病患者血糖控制不佳会促使眼部并发症如DR的发生。