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生物信息学与系统生物学方法用于识别银屑病与心血管疾病之间的致病联系。

Bioinformatics and Systems Biology Approach to Identify the Pathogenetic Link Between Psoriasis and Cardiovascular Disease.

作者信息

Shi Liping, Du Xiaoqing, Li Jing, Zhang Guoqiang

机构信息

Department of Dermatology, The First Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.

Candidate Branch of National Clinical Research Center for Skin Diseases, Shijiazhuang, People's Republic of China.

出版信息

Clin Cosmet Investig Dermatol. 2023 Aug 22;16:2283-2295. doi: 10.2147/CCID.S421193. eCollection 2023.

DOI:10.2147/CCID.S421193
PMID:37635735
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10460209/
Abstract

OBJECTIVE

This study aimed to identify hub genes and common pathways shared between psoriasis and cardiovascular disease (CVD) using bioinformatics analysis and predict the transcription factors (TFs) of hub genes.

METHODS

GSE133555 data from the Gene Expression Omnibus (GEO) database were used to identify differentially expressed genes (DEGs) between involved and uninvolved skin lesions in psoriasis, employing the limma package in R. Additionally, CVD-related genes were obtained from the GeneCards database. The intersection of DEGs and CVD-related genes yielded CVD-DEGs. Gene Ontology and signaling pathway analyses were performed using the clusterProfiler package in R. Hub genes were identified by intersecting six algorithms in the CytoHubba plugin of Cytoscape. To identify potential biomarkers, the GSE14905 dataset was subjected to receiver operating characteristic analysis, resulting in the identification of eight central hub genes. Finally, the NetworkAnalyst web tool was used to identify the TFs of the eight hub genes.

RESULTS

We identified 92 significant DEGs out of 1825 CVD-related genes in psoriasis obtained from the GSE13355 and GeneCard data. Functional enrichment analysis revealed the involvement of these genes in various signaling pathways, including the interleukin-17 signaling, tumor necrosis factor signaling, lipid and atherosclerosis, chemokine signaling, and cytokine signaling pathways in the immune system. The eight hub genes identified included interleukin-1 beta, C-X-C motif chemokine ligand 8, signal transducer and activator of transcription 3, C-C motif chemokine ligand 2, arginase 1, C-X-C motif chemokine receptor 4, cyclin D1, and matrix metallopeptidase 9, with forkhead box C1 also identified as an associated TF of these genes. These hub genes and TF may act as key regulators in the context of CVD.

CONCLUSION

This study identified several hub genes and signaling pathways associated with both CVD and psoriasis. These findings lay the groundwork for potential therapeutic interventions for patients with psoriasis affected by CVD.

摘要

目的

本研究旨在通过生物信息学分析确定银屑病与心血管疾病(CVD)之间共享的枢纽基因和共同通路,并预测枢纽基因的转录因子(TFs)。

方法

使用来自基因表达综合数据库(GEO)的GSE133555数据,通过R语言中的limma包来鉴定银屑病中受累皮肤病变和未受累皮肤病变之间的差异表达基因(DEGs)。此外,从基因卡片数据库中获取与CVD相关的基因。DEGs与CVD相关基因的交集产生了CVD-DEGs。使用R语言中的clusterProfiler包进行基因本体论和信号通路分析。通过在Cytoscape的CytoHubba插件中交叉六种算法来鉴定枢纽基因。为了鉴定潜在的生物标志物,对GSE14905数据集进行了受试者工作特征分析,从而鉴定出八个核心枢纽基因。最后,使用网络分析工具(NetworkAnalyst)来鉴定这八个枢纽基因的TFs。

结果

我们从GSE13355和基因卡片数据中获得的银屑病的1825个与CVD相关的基因中鉴定出92个显著的DEGs。功能富集分析表明这些基因参与了各种信号通路,包括白细胞介素-17信号通路、肿瘤坏死因子信号通路、脂质与动脉粥样硬化、趋化因子信号通路以及免疫系统中的细胞因子信号通路。鉴定出的八个枢纽基因包括白细胞介素-1β、C-X-C基序趋化因子配体8、信号转导和转录激活因子3、C-C基序趋化因子配体2、精氨酸酶1、C-X-C基序趋化因子受体4、细胞周期蛋白D1和基质金属蛋白酶9,叉头框C1也被鉴定为这些基因的相关TF。这些枢纽基因和TF可能在CVD的背景下充当关键调节因子。

结论

本研究鉴定出了几个与CVD和银屑病相关的枢纽基因和信号通路。这些发现为患有CVD的银屑病患者的潜在治疗干预奠定了基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90d7/10460209/32b02a50409a/CCID-16-2283-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90d7/10460209/8f079c4a6283/CCID-16-2283-g0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90d7/10460209/71748e194818/CCID-16-2283-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90d7/10460209/32b02a50409a/CCID-16-2283-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90d7/10460209/8f079c4a6283/CCID-16-2283-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90d7/10460209/b4d8560fa14d/CCID-16-2283-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90d7/10460209/3f914964371c/CCID-16-2283-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90d7/10460209/275d4de482b9/CCID-16-2283-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90d7/10460209/71748e194818/CCID-16-2283-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90d7/10460209/32b02a50409a/CCID-16-2283-g0006.jpg

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