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瘢痕疙瘩相关关键基因及通路的生物信息学分析。

Bioinformatic Analysis of Key Genes and Pathways Related to Keloids.

机构信息

West China School of Medicine, Sichuan University, Chengdu, Sichuan 610041, China.

Department of Burn and Plastic Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.

出版信息

Biomed Res Int. 2021 Mar 23;2021:5897907. doi: 10.1155/2021/5897907. eCollection 2021.

Abstract

BACKGROUND

The pathophysiology of keloids is complex, and the treatment for keloids is still an unmet medical need. Our study is aimed at identifying the hub genes among the differentially expressed genes (DEGs) between normal skin tissue and keloids and key pathways in the development of keloids.

MATERIALS AND METHODS

We downloaded the GSE92566 and GSE90051 microarray data, which contain normal skin tissue and keloid gene expression data. GSE92566 was treated as a discovery dataset for summarizing the significantly DEGs, and GSE90051 served as a validation dataset. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes pathway, Reactome enrichment analysis, gene set enrichment analysis, and gene set variation analysis were performed for the key functions and pathways enriched in DEGs. Moreover, we also validated the hub genes identified from the protein-protein interaction network and predicted miRNA-hub gene interactions.

RESULTS

117 downregulated DEGs and 204 upregulated DEGs in GSE92566 were identified. Extracellular and collagen-related pathways were prominent in upregulated DEGs, while the keratinization-related pathway was associated with downregulated DEGs. The hub genes included COL5A1, COL5A2, and SERPINH1, which were also validated in GSE90051.

CONCLUSION

This study identified several hub genes and provided insights for the underlying pathways and miRNA-hub gene interactions for keloid development through bioinformatic analysis of two microarray datasets. Additionally, our results would support the development of future therapeutic strategies.

摘要

背景

瘢痕疙瘩的发病机制复杂,瘢痕疙瘩的治疗仍是未满足的医学需求。本研究旨在鉴定正常皮肤组织和瘢痕疙瘩之间差异表达基因(DEGs)中的关键基因,并分析瘢痕疙瘩发生发展的关键途径。

材料与方法

下载 GSE92566 和 GSE90051 微阵列数据集,其中包含正常皮肤组织和瘢痕疙瘩基因表达数据。GSE92566 被视为汇总显著 DEGs 的发现数据集,GSE90051 则作为验证数据集。对 DEGs 中富集的关键功能和途径进行基因本体论、京都基因与基因组百科全书通路、Reactome 富集分析、基因集富集分析和基因集变异分析。此外,我们还验证了从蛋白质-蛋白质相互作用网络中识别的关键基因,并预测了 miRNA-关键基因相互作用。

结果

在 GSE92566 中鉴定出 117 个下调 DEGs 和 204 个上调 DEGs。上调 DEGs 中突出的是细胞外和胶原相关途径,而下调 DEGs 与角化相关途径相关。关键基因包括 COL5A1、COL5A2 和 SERPINH1,在 GSE90051 中也得到了验证。

结论

本研究通过对两个微阵列数据集的生物信息学分析,鉴定了几个关键基因,并为瘢痕疙瘩发生发展的潜在途径和 miRNA-关键基因相互作用提供了见解。此外,我们的研究结果将支持未来治疗策略的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c36d/8009712/a85dc56c6bf7/BMRI2021-5897907.001.jpg

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