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单细胞转录组分析揭示糖尿病视网膜病变中视网膜细胞亚群水平的变化及相关通路。

Single-cell transcriptomic analysis revealing changes in retinal cell subpopulation levels and the pathways involved in diabetic retinopathy.

作者信息

Zhang Rui, Huang Chengyu, Chen Yixuan, Li Ting, Pang Long

机构信息

Department of Ophthalmology, The Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou, China.

Yuan Dong International Academy of Life Sciences, Nanning, China.

出版信息

Ann Transl Med. 2022 May;10(10):562. doi: 10.21037/atm-22-1546.

DOI:10.21037/atm-22-1546
PMID:35722432
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9201190/
Abstract

BACKGROUND

Diabetic retinopathy (DR) is a common microvascular complication of diabetes and one of the most common causes of visual impairment and blindness. However, it is not yet known how abnormal retinal cell subpopulations contribute to disease progression.

METHODS

In this study, we used the Gene Expression Omnibus database to construct a single-cell atlas of DR and healthy samples to explore changes in the abundance of different cell subpopulations, and identify the molecular pathways potentially involved in DR.

RESULTS

Our results showed that DR was associated with significantly reduced numbers of bipolar cells, Müller glia, retinal pigment epithelial cells, and cone photoreceptors, but was also associated with significantly greater numbers of pericytes, rod photoreceptors, anaplastic cells, and microglia. Our results suggest that subpopulations of Müller glia, microglia, endothelial cells, and bipolar cells in DR tissues may be involved in various oxidative stress- and inflammation-related pathways.

CONCLUSIONS

In summary, we showed that Müller glia, endothelial cells, microglia, and bipolar cells in DR tissues are involved in oxidative stress- and inflammation-related pathways, which may contribute to the progression of the disease and ultimately lead to visual impairment and blindness. This study will provide a theoretical basis for further exploring the specific mechanism of DR.

摘要

背景

糖尿病视网膜病变(DR)是糖尿病常见的微血管并发症,也是视力损害和失明的最常见原因之一。然而,目前尚不清楚视网膜细胞亚群异常如何促进疾病进展。

方法

在本研究中,我们使用基因表达综合数据库构建DR和健康样本的单细胞图谱,以探索不同细胞亚群丰度的变化,并确定可能参与DR的分子途径。

结果

我们的结果表明,DR与双极细胞、Müller胶质细胞、视网膜色素上皮细胞和视锥光感受器数量显著减少有关,但也与周细胞、视杆光感受器、间变细胞和小胶质细胞数量显著增加有关。我们的结果表明,DR组织中的Müller胶质细胞、小胶质细胞、内皮细胞和双极细胞亚群可能参与各种氧化应激和炎症相关途径。

结论

总之,我们表明DR组织中的Müller胶质细胞、内皮细胞、小胶质细胞和双极细胞参与氧化应激和炎症相关途径,这可能有助于疾病进展并最终导致视力损害和失明。本研究将为进一步探索DR的具体机制提供理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ac/9201190/e566694102e9/atm-10-10-562-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ac/9201190/a4f23c7c11ba/atm-10-10-562-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ac/9201190/cf8b5eedc6f6/atm-10-10-562-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ac/9201190/a4f80dd2e13c/atm-10-10-562-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ac/9201190/08bbbe264722/atm-10-10-562-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ac/9201190/e566694102e9/atm-10-10-562-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ac/9201190/a4f23c7c11ba/atm-10-10-562-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ac/9201190/cf8b5eedc6f6/atm-10-10-562-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ac/9201190/a4f80dd2e13c/atm-10-10-562-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ac/9201190/08bbbe264722/atm-10-10-562-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ac/9201190/e566694102e9/atm-10-10-562-f5.jpg

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