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糖尿病视网膜神经变性中的硫氧还蛋白相互作用蛋白:糖尿病视网膜病变的新型潜在治疗靶点。

Thioredoxin-interacting protein in diabetic retinal neurodegeneration: A novel potential therapeutic target for diabetic retinopathy.

作者信息

Liu Chengzhi, Dong Wenkang, Lv Zhengshuai, Kong Li, Ren Xiang

机构信息

The First Affiliated Hospital of Dalian Medical University, Dalian, China.

Department of Histology and Embryology, College of Basic Medicine, Dalian Medical University, Dalian, China.

出版信息

Front Neurosci. 2022 Aug 9;16:957667. doi: 10.3389/fnins.2022.957667. eCollection 2022.

DOI:10.3389/fnins.2022.957667
PMID:36017183
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9396221/
Abstract

Diabetic retinopathy (DR) is a common complication of diabetes mellitus and has been considered a microvascular disease for a long time. However, recent evidence suggests that diabetic retinal neurodegeneration (DRN), which manifests as neuronal apoptosis, a decrease in optic nerve axons, and reactive gliosis, occurs prior to retinal microvascular alterations. Thioredoxin-interacting protein (TXNIP) is an endogenous inhibitor of thioredoxin (Trx), and it acts by inhibiting its reducing capacity, thereby promoting cellular oxidative stress. In addition, it participates in regulating multiple signaling pathways as a member of the α-arrestin family of proteins. Accumulating evidence suggests that TXNIP is upregulated in diabetes and plays a pivotal role in the pathophysiological process of DR. In this review, we summarized the role of TXNIP in DRN, aiming to provide evidence for DR treatment in the future.

摘要

糖尿病性视网膜病变(DR)是糖尿病的常见并发症,长期以来一直被认为是一种微血管疾病。然而,最近的证据表明,糖尿病性视网膜神经变性(DRN),表现为神经元凋亡、视神经轴突减少和反应性胶质细胞增生,发生在视网膜微血管改变之前。硫氧还蛋白相互作用蛋白(TXNIP)是硫氧还蛋白(Trx)的内源性抑制剂,它通过抑制其还原能力发挥作用,从而促进细胞氧化应激。此外,它作为α- arrestin蛋白家族的成员参与调节多种信号通路。越来越多的证据表明,TXNIP在糖尿病中上调,并在DR的病理生理过程中起关键作用。在本综述中,我们总结了TXNIP在DRN中的作用,旨在为未来DR的治疗提供证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f73f/9396221/f5cc214839ce/fnins-16-957667-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f73f/9396221/f5cc214839ce/fnins-16-957667-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f73f/9396221/f5cc214839ce/fnins-16-957667-g001.jpg

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本文引用的文献

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Diabetes Res Clin Pract. 2022 Mar;185:109788. doi: 10.1016/j.diabres.2022.109788. Epub 2022 Feb 17.
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Potential Combination Drug Therapy to Prevent Redox Stress and Mitophagy Dysregulation in Retinal Müller Cells under High Glucose Conditions: Implications for Diabetic Retinopathy.高糖条件下预防视网膜Müller细胞氧化还原应激和线粒体自噬失调的潜在联合药物治疗:对糖尿病视网膜病变的意义
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SRY 框转录因子 9 通过上调 TXNIP 转录来调节糖尿病视网膜病变中的 Müller 细胞胶质增生。
Exp Anim. 2023 Aug 7;72(3):302-313. doi: 10.1538/expanim.22-0126. Epub 2023 Jan 16.
MiR-17-5p Inhibits TXNIP/NLRP3 Inflammasome Pathway and Suppresses Pancreatic β-Cell Pyroptosis in Diabetic Mice.
微小RNA-17-5p抑制TXNIP/NLRP3炎性小体途径并抑制糖尿病小鼠胰腺β细胞焦亡
Front Cardiovasc Med. 2021 Nov 22;8:768029. doi: 10.3389/fcvm.2021.768029. eCollection 2021.
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TXNIP interaction with GLUT1 depends on PI(4,5)P.TXNIP 与 GLUT1 的相互作用依赖于 PI(4,5)P。
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