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转基因小鼠在白内障分子发病机制中的应用。

Application of transgenic mice to the molecular pathogenesis of cataract.

作者信息

Zhang Yue, Chen Xiao-Ya, Hu Yu-Zhu, Zhang Xiao, Zheng Shun-Fei, Hu Shan-Shan

机构信息

Mudanjiang Medical University, Mudanjiang 157011, Heilongjiang Province, China.

Department of Ophthalmology, Hongqi Hospital of Mudanjiang Medical University, Mudanjiang 157011, Heilongjiang Province, China.

出版信息

Int J Ophthalmol. 2024 Oct 18;17(10):1929-1948. doi: 10.18240/ijo.2024.10.21. eCollection 2024.

DOI:10.18240/ijo.2024.10.21
PMID:39430018
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11422363/
Abstract

One of the most prevalent disorders that cause blindness worldwide is cataract, and its essence is the visual disorder caused by the opacity of the lens. The significant degree of variation in cataracts and the fact that a variety of factors can impact a patient's lens transparency make it especially crucial to investigate the pathogenesis of cataracts at the molecular level. It has been found that more than 60 genes are linked to the formation of cataracts, and the construction of a transgenic mouse model of cataract similar to the selection of human lens clouding due to a variety of causes has become an important means of studying the pathogenesis of cataract. Therefore, the research on the application of transgenic mice to the molecular pathogenesis of cataracts will be the main topic of this review of the literature.

摘要

白内障是全球范围内导致失明的最常见疾病之一,其实质是由晶状体混浊引起的视觉障碍。白内障的显著程度差异以及多种因素会影响患者晶状体透明度这一事实,使得在分子水平上研究白内障的发病机制尤为关键。现已发现60多个基因与白内障的形成有关,构建类似于人类因多种原因导致晶状体混浊的白内障转基因小鼠模型,已成为研究白内障发病机制的重要手段。因此,转基因小鼠在白内障分子发病机制中的应用研究将是本文献综述的主要主题。

相似文献

1
Application of transgenic mice to the molecular pathogenesis of cataract.转基因小鼠在白内障分子发病机制中的应用。
Int J Ophthalmol. 2024 Oct 18;17(10):1929-1948. doi: 10.18240/ijo.2024.10.21. eCollection 2024.
2
Lipid peroxidation and cataracts: N-acetylcarnosine as a therapeutic tool to manage age-related cataracts in human and in canine eyes.脂质过氧化与白内障:N-乙酰肌肽作为治疗人类和犬类年龄相关性白内障的一种治疗手段。
Drugs R D. 2004;5(3):125-39. doi: 10.2165/00126839-200405030-00001.
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Participation of Lens Proteins and miRs in Traumatic and Inheritance Cataract: A Review on Diagnostic and Therapeutic Approaches for Cataract Management.晶状体蛋白和微小RNA在创伤性和遗传性白内障中的作用:白内障治疗的诊断和治疗方法综述
Curr Pharm Biotechnol. 2024 Jun 25. doi: 10.2174/0113892010303094240613105517.
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Potentiation of intraocular absorption and drug metabolism of N-acetylcarnosine lubricant eye drops: drug interaction with sight threatening lipid peroxides in the treatment for age-related eye diseases.N-乙酰肌肽润滑滴眼液的眼内吸收及药物代谢增强作用:在年龄相关性眼病治疗中药物与威胁视力的脂质过氧化物的相互作用
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A transgenic animal model of osmotic cataract. Part 1: over-expression of bovine Na+/myo-inositol cotransporter in lens fibers.渗透性白内障的转基因动物模型。第1部分:牛Na⁺/肌醇共转运蛋白在晶状体纤维中的过表达。
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本文引用的文献

1
miR-26 Deficiency Causes Alterations in Lens Transcriptome and Results in Adult-Onset Cataract.miR-26 缺失导致晶状体转录组发生改变,从而导致成年期白内障。
Invest Ophthalmol Vis Sci. 2024 Apr 1;65(4):42. doi: 10.1167/iovs.65.4.42.
2
Comparison of two methods of sperm- and testis-mediated gene transfer in production of transgenic animals: A systematic review.转基因动物生产中精子介导和睾丸介导基因转移两种方法的比较:一项系统综述。
Anim Genet. 2024 Jun;55(3):328-343. doi: 10.1111/age.13404. Epub 2024 Feb 15.
3
Glutaredoxin 2 protects lens epithelial cells from epithelial-mesenchymal transition by suppressing mitochondrial oxidative stress-related upregulation of integrin-linked kinase.谷氧还蛋白 2 通过抑制整合素连接激酶的线粒体氧化应激相关上调来保护晶状体上皮细胞免于上皮-间充质转化。
Exp Eye Res. 2023 Sep;234:109609. doi: 10.1016/j.exer.2023.109609. Epub 2023 Aug 2.
4
Endoplasmic Reticulum Stress and the Lysosomal Pathway Play Crucial Roles in the Progression of βB2-Crystallin Mutation-Induced Congenital Cataracts in Mice.内质网应激和溶酶体途径在βB2-晶体蛋白突变诱导的小鼠先天性白内障的进展中发挥关键作用。
Invest Ophthalmol Vis Sci. 2023 Apr 3;64(4):34. doi: 10.1167/iovs.64.4.34.
5
TGF-β/Smad Signalling Activation by HTRA1 Regulates the Function of Human Lens Epithelial Cells and Its Mechanism in Posterior Subcapsular Congenital Cataract.HTRA1 通过 TGF-β/Smad 信号通路激活调控人晶状体上皮细胞的功能及其在后发性白内障中的作用机制。
Int J Mol Sci. 2022 Nov 20;23(22):14431. doi: 10.3390/ijms232214431.
6
Transgenic Mouse Models to Study the Development and Maintenance of the Adrenal Cortex.研究肾上腺皮质发育和维持的转基因小鼠模型。
Int J Mol Sci. 2022 Nov 19;23(22):14388. doi: 10.3390/ijms232214388.
7
Deficiency of Jamc Leads to Congenital Nuclear Cataract and Activates the Unfolded Protein Response in Mouse Lenses.Jamc 缺乏导致先天性核白内障,并激活小鼠晶状体中的未折叠蛋白反应。
Invest Ophthalmol Vis Sci. 2022 Sep 1;63(10):1. doi: 10.1167/iovs.63.10.1.
8
The many problems of somatic cell nuclear transfer in reproductive cloning of mammals.哺乳动物生殖性克隆中体细胞核移植的诸多问题。
Theriogenology. 2022 Sep 1;189:246-254. doi: 10.1016/j.theriogenology.2022.06.030. Epub 2022 Jun 30.
9
The protective mechanism of Grx2 in ultraviolet-B (UVB)-induced cataract formation.谷氧还蛋白 2 在紫外线 B(UVB)诱导白内障形成中的保护机制。
Biochem Biophys Res Commun. 2022 Jul 12;613:107-112. doi: 10.1016/j.bbrc.2022.04.056. Epub 2022 Apr 25.
10
GPX1 knockout, not catalase knockout, causes accelerated abnormal optical aberrations and cataract in the aging lens.GPX1 基因敲除而非 catalase 基因敲除导致衰老晶状体中异常光学像差和白内障的加速形成。
Mol Vis. 2022 Feb 22;28:11-20. eCollection 2022.