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鉴定免疫浸润相关的竞争性内源RNA作为原发性开角型青光眼患者预后的新型生物标志物

Identification of Immune Infiltration-Related ceRNAs as Novel Biomarkers for Prognosis of Patients With Primary Open-Angle Glaucoma.

作者信息

Zhang Daowei, Wu Jiawen, Zhang Shenghai, Wu Jihong

机构信息

Eye and ENT Hospital, College of Medicine, Eye Institute, Fudan University, Shanghai, China.

Shanghai Key Laboratory of Visual Impairment and Restoration, Science and Technology Commission of Shanghai Municipality, Shanghai, China.

出版信息

Front Genet. 2022 May 27;13:838220. doi: 10.3389/fgene.2022.838220. eCollection 2022.

DOI:10.3389/fgene.2022.838220
PMID:35692841
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9184720/
Abstract

Glaucoma is the leading cause of irreversible blindness globally; hence, relevant clinical biomarkers are necessary to enable diagnosis, early detection, and development of novel therapies. The differentially expressed genes were annotated and visualized using Gene Ontology and Kyoto Encyclopedia. In addition, a competitive endogenous ribonucleic acids network was constructed using Cytoscape, which explained the regulation of gene expression in glaucoma. The CIBERSORT algorithm was employed to analyze the immune microenvironment. We validated that the core genes could predict glaucoma occurrence and development and identified potential molecular mechanism pathways, which were associated with immune infiltration and participated in endogenous regulation networks. Our data may partially explain the pathogenesis of glaucoma and they provide potential theoretical support for targeted therapy.

摘要

青光眼是全球不可逆失明的主要原因;因此,相关的临床生物标志物对于诊断、早期检测和新型疗法的开发至关重要。使用基因本体论和京都基因与基因组百科全书对差异表达基因进行注释和可视化。此外,利用Cytoscape构建了竞争性内源性核糖核酸网络,该网络解释了青光眼基因表达的调控。采用CIBERSORT算法分析免疫微环境。我们验证了核心基因可以预测青光眼的发生和发展,并确定了潜在的分子机制途径,这些途径与免疫浸润相关并参与内源性调控网络。我们的数据可能部分解释了青光眼的发病机制,并为靶向治疗提供了潜在的理论支持。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aab8/9184720/131811826216/fgene-13-838220-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aab8/9184720/cc5f64543dc8/fgene-13-838220-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aab8/9184720/18950e01c2d3/fgene-13-838220-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aab8/9184720/5c3d9fa48404/fgene-13-838220-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aab8/9184720/295f785fa5a7/fgene-13-838220-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aab8/9184720/2bfe51279e37/fgene-13-838220-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aab8/9184720/131811826216/fgene-13-838220-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aab8/9184720/cc5f64543dc8/fgene-13-838220-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aab8/9184720/18950e01c2d3/fgene-13-838220-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aab8/9184720/5c3d9fa48404/fgene-13-838220-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aab8/9184720/295f785fa5a7/fgene-13-838220-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aab8/9184720/2bfe51279e37/fgene-13-838220-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aab8/9184720/131811826216/fgene-13-838220-g006.jpg

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Energy Metabolism in the Inner Retina in Health and Glaucoma.
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Deregulated lncRNA MAGI2-AS3 in Alzheimer's disease attenuates amyloid-β induced neurotoxicity and neuroinflammation by sponging miR-374b-5p.阿尔茨海默病中失调的 lncRNA MAGI2-AS3 通过海绵吸附 miR-374b-5p 减轻淀粉样β诱导的神经毒性和神经炎症。
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