Analysis of Inflammation-Related Genes in Patients with Stanford Type A Aortic Dissection

<b>Background:</b> Aortic dissection (AD) is a life-threatening cardiovascular disease. Pathophysiologically, it has been shown that aortic wall inflammation promotes the occurrence and development of aortic dissection. Thus, the aim of the current research was to determine the inflammat...

Full description

Bibliographic Details
Main Authors: Lin Li, Ziwei Zeng, Vugar Yagublu, Nuh Rahbari, Christoph Reißfelder, Michael Keese
Format: Article
Language:English
Published: MDPI AG 2023-06-01
Series:Journal of Personalized Medicine
Subjects:
Online Access:https://www.mdpi.com/2075-4426/13/6/990
_version_ 1797593918553980928
author Lin Li
Ziwei Zeng
Vugar Yagublu
Nuh Rahbari
Christoph Reißfelder
Michael Keese
author_facet Lin Li
Ziwei Zeng
Vugar Yagublu
Nuh Rahbari
Christoph Reißfelder
Michael Keese
author_sort Lin Li
collection DOAJ
description <b>Background:</b> Aortic dissection (AD) is a life-threatening cardiovascular disease. Pathophysiologically, it has been shown that aortic wall inflammation promotes the occurrence and development of aortic dissection. Thus, the aim of the current research was to determine the inflammation-related biomarkers in AD. <b>Methods:</b> In this study, we conducted differentially expressed genes (DEGs) analysis using the GSE153434 dataset containing 10 type A aortic dissection (TAAD) and 10 normal samples downloaded from the Gene Expression Omnibus (GEO) database. The intersection of DEGs and inflammation-related genes was identified as differential expressed inflammation-related genes (DEIRGs). Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed for DEIRGs. We then constructed the protein–protein interaction (PPI) network using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database and identified hub genes using the Cytoscape plugin MCODE. Finally, least absolute shrinkage and selection operator (LASSO) logistic regression was used to construct a diagnostic model. <b>Results:</b> A total of 1728 DEGs were identified between the TAAD and normal samples. Thereafter, 61 DEIRGs are obtained by taking the intersection of DEGs and inflammation-related genes. The GO indicated that DEIRGs were mainly enriched in response to lipopolysaccharide, in response to molecules of bacterial origin, secretory granule membrane, external side of plasma, receptor ligand activity, and signaling receptor activator activity. KEGG analysis indicated that DEIRGs were mainly enriched in cytokine–cytokine receptor interaction, TNF signaling pathway, and proteoglycans in cancer. We identified <i>MYC</i>, <i>SELL</i>, <i>HIF1A</i>, <i>EDN1</i>, <i>SERPINE1</i>, <i>CCL20</i>, <i>IL1R1</i>, <i>NOD2</i>, <i>TLR2</i>, <i>CD69</i>, <i>PLAUR</i>, <i>MMP14</i>, and <i>HBEGF</i> as hub genes using the MCODE plug-in. The ROC indicated these genes had a good diagnostic performance for TAAD. <b>Conclusion:</b> In conclusion, our study identified 13 hub genes in the TAAD. This study will be of significance for the future development of a preventive therapy of TAAD.
first_indexed 2024-03-11T02:15:20Z
format Article
id doaj.art-4c3ac95d28de4a0697416b2774159943
institution Directory Open Access Journal
issn 2075-4426
language English
last_indexed 2024-03-11T02:15:20Z
publishDate 2023-06-01
publisher MDPI AG
record_format Article
series Journal of Personalized Medicine
spelling doaj.art-4c3ac95d28de4a0697416b27741599432023-11-18T11:11:34ZengMDPI AGJournal of Personalized Medicine2075-44262023-06-0113699010.3390/jpm13060990Analysis of Inflammation-Related Genes in Patients with Stanford Type A Aortic DissectionLin Li0Ziwei Zeng1Vugar Yagublu2Nuh Rahbari3Christoph Reißfelder4Michael Keese5Department of Vascular Surgery, Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, GermanyDepartment of Vascular Surgery, Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, GermanySurgical Clinic Mannheim, Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, GermanySurgical Clinic Mannheim, Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, GermanySurgical Clinic Mannheim, Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, GermanyEuropean Center of Angioscience ECAS, Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany<b>Background:</b> Aortic dissection (AD) is a life-threatening cardiovascular disease. Pathophysiologically, it has been shown that aortic wall inflammation promotes the occurrence and development of aortic dissection. Thus, the aim of the current research was to determine the inflammation-related biomarkers in AD. <b>Methods:</b> In this study, we conducted differentially expressed genes (DEGs) analysis using the GSE153434 dataset containing 10 type A aortic dissection (TAAD) and 10 normal samples downloaded from the Gene Expression Omnibus (GEO) database. The intersection of DEGs and inflammation-related genes was identified as differential expressed inflammation-related genes (DEIRGs). Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed for DEIRGs. We then constructed the protein–protein interaction (PPI) network using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database and identified hub genes using the Cytoscape plugin MCODE. Finally, least absolute shrinkage and selection operator (LASSO) logistic regression was used to construct a diagnostic model. <b>Results:</b> A total of 1728 DEGs were identified between the TAAD and normal samples. Thereafter, 61 DEIRGs are obtained by taking the intersection of DEGs and inflammation-related genes. The GO indicated that DEIRGs were mainly enriched in response to lipopolysaccharide, in response to molecules of bacterial origin, secretory granule membrane, external side of plasma, receptor ligand activity, and signaling receptor activator activity. KEGG analysis indicated that DEIRGs were mainly enriched in cytokine–cytokine receptor interaction, TNF signaling pathway, and proteoglycans in cancer. We identified <i>MYC</i>, <i>SELL</i>, <i>HIF1A</i>, <i>EDN1</i>, <i>SERPINE1</i>, <i>CCL20</i>, <i>IL1R1</i>, <i>NOD2</i>, <i>TLR2</i>, <i>CD69</i>, <i>PLAUR</i>, <i>MMP14</i>, and <i>HBEGF</i> as hub genes using the MCODE plug-in. The ROC indicated these genes had a good diagnostic performance for TAAD. <b>Conclusion:</b> In conclusion, our study identified 13 hub genes in the TAAD. This study will be of significance for the future development of a preventive therapy of TAAD.https://www.mdpi.com/2075-4426/13/6/990TAADhub geneinflammation-related genes
spellingShingle Lin Li
Ziwei Zeng
Vugar Yagublu
Nuh Rahbari
Christoph Reißfelder
Michael Keese
Analysis of Inflammation-Related Genes in Patients with Stanford Type A Aortic Dissection
Journal of Personalized Medicine
TAAD
hub gene
inflammation-related genes
title Analysis of Inflammation-Related Genes in Patients with Stanford Type A Aortic Dissection
title_full Analysis of Inflammation-Related Genes in Patients with Stanford Type A Aortic Dissection
title_fullStr Analysis of Inflammation-Related Genes in Patients with Stanford Type A Aortic Dissection
title_full_unstemmed Analysis of Inflammation-Related Genes in Patients with Stanford Type A Aortic Dissection
title_short Analysis of Inflammation-Related Genes in Patients with Stanford Type A Aortic Dissection
title_sort analysis of inflammation related genes in patients with stanford type a aortic dissection
topic TAAD
hub gene
inflammation-related genes
url https://www.mdpi.com/2075-4426/13/6/990
work_keys_str_mv AT linli analysisofinflammationrelatedgenesinpatientswithstanfordtypeaaorticdissection
AT ziweizeng analysisofinflammationrelatedgenesinpatientswithstanfordtypeaaorticdissection
AT vugaryagublu analysisofinflammationrelatedgenesinpatientswithstanfordtypeaaorticdissection
AT nuhrahbari analysisofinflammationrelatedgenesinpatientswithstanfordtypeaaorticdissection
AT christophreißfelder analysisofinflammationrelatedgenesinpatientswithstanfordtypeaaorticdissection
AT michaelkeese analysisofinflammationrelatedgenesinpatientswithstanfordtypeaaorticdissection