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通过激活Nrf2预防糖尿病并发症:糖尿病性心肌病和肾病

Prevention of diabetic complications by activation of Nrf2: diabetic cardiomyopathy and nephropathy.

作者信息

Li Bing, Liu Shujun, Miao Lining, Cai Lu

机构信息

Department of Nephrology, Second Hospital of Jilin University, Changchun 130042, China.

出版信息

Exp Diabetes Res. 2012;2012:216512. doi: 10.1155/2012/216512. Epub 2012 May 8.

DOI:10.1155/2012/216512
PMID:22645602
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3356887/
Abstract

Diabetic cardiomyopathy and nephropathy are two major causes of death of patients with diabetes. Extra generation of reactive oxygen species (ROS), induced by hyperglycemia, is considered as the main reason for the development of these diabetic complications. Transcription factor, NFE2-related factor 2 (Nrf2), is a master regulator of cellular detoxification response and redox status, and also provides a protective action from various oxidative stresses and damages. Recently we have demonstrated its important role in determining the susceptibility of cells or tissues to diabetes-induced oxidative stress and/or damage. Therefore, this review will specifically summarize the information available regarding the effect of Nrf2 on the diabetic complications with a focus on diabetic cardiomyopathy and nephropathy. Given the feature that Nrf2 is easily induced by several compounds, we also discussed the role of different Nrf2 activators in the prevention or therapy of various diabetic complications. These findings suggest that Nrf2 has a potential application in the clinic setting for diabetic patients in the short future.

摘要

糖尿病性心肌病和肾病是糖尿病患者的两大主要死因。高血糖诱导产生的额外活性氧(ROS)被认为是这些糖尿病并发症发生发展的主要原因。转录因子NFE2相关因子2(Nrf2)是细胞解毒反应和氧化还原状态的主要调节因子,也能对各种氧化应激和损伤起到保护作用。最近我们已经证明了它在决定细胞或组织对糖尿病诱导的氧化应激和/或损伤的易感性方面的重要作用。因此,本综述将特别总结关于Nrf2对糖尿病并发症影响的现有信息,重点关注糖尿病性心肌病和肾病。鉴于Nrf2容易被几种化合物诱导的特性,我们还讨论了不同Nrf2激活剂在预防或治疗各种糖尿病并发症中的作用。这些发现表明,Nrf2在不久的将来在糖尿病患者的临床治疗中具有潜在应用价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/370d/3356887/866393f0c431/EDR2012-216512.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/370d/3356887/dd782b7daf99/EDR2012-216512.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/370d/3356887/866393f0c431/EDR2012-216512.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/370d/3356887/dd782b7daf99/EDR2012-216512.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/370d/3356887/866393f0c431/EDR2012-216512.002.jpg

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