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Nrf2,一种针对角膜疾病氧化应激的潜在治疗靶点。

Nrf2, a Potential Therapeutic Target against Oxidative Stress in Corneal Diseases.

机构信息

Department of Ophthalmology, The First Hospital of Jilin University, Jilin, China.

Department of Radiology, The First Hospital of Jilin University, Jilin, China.

出版信息

Oxid Med Cell Longev. 2017;2017:2326178. doi: 10.1155/2017/2326178. Epub 2017 Oct 25.

DOI:10.1155/2017/2326178
PMID:29209447
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5676473/
Abstract

Corneal diseases are one of the major causes of blindness worldwide. Conservative medical agents, which may prevent sight-threatening corneal disease progression, are urgently desired. Numerous evidences have revealed the involvement of oxidative stress in various corneal diseases, such as corneal wound healing and Fuchs endothelial corneal dystrophy (FECD). Nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/Kelch-like erythroid-cell-derived protein with CNC homology- (ECH-) associated protein 1 (Keap1)/antioxidant response element (ARE) signaling is well known as one of the main antioxidative defense systems. To the best of our knowledge, this is the first review to elucidate the different expression profiles of Nrf2 signaling as well as the underlying mechanisms in corneal diseases, implicating that Nrf2 may serve as a potentially promising therapeutic target for corneal diseases.

摘要

角膜疾病是全球致盲的主要原因之一。人们迫切需要具有预防威胁视力的角膜疾病进展作用的保守医学药物。大量证据表明氧化应激参与了各种角膜疾病,如角膜创伤愈合和 Fuchs 内皮角膜营养不良(FECD)。核因子(红系衍生 2)样 2(Nrf2)/Kelch 样红细胞衍生蛋白与 CNC 同源(ECH)相关蛋白 1(Keap1)/抗氧化反应元件(ARE)信号通路是众所周知的主要抗氧化防御系统之一。据我们所知,这是第一篇阐明 Nrf2 信号在角膜疾病中的不同表达谱及其潜在机制的综述,表明 Nrf2 可能成为治疗角膜疾病的有潜力的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4053/5676473/cb6c49f901a1/OMCL2017-2326178.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4053/5676473/8ae92e78fc8e/OMCL2017-2326178.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4053/5676473/cb6c49f901a1/OMCL2017-2326178.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4053/5676473/8ae92e78fc8e/OMCL2017-2326178.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4053/5676473/cb6c49f901a1/OMCL2017-2326178.002.jpg

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