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Expression Pattern and Molecular Mechanism of Oxidative Stress-Related Genes in Myocardial Ischemia–Reperfusion Injury
(1) Background: The molecular mechanism of oxidative stress-related genes (OSRGs) in myocardial ischemia–reperfusion injury (MIRI) has not been fully elucidated. (2) Methods: Differential expression analysis, enrichment analysis, and PPI analysis were performed on the MIRI-related datasets GSE160516...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9961140/ https://www.ncbi.nlm.nih.gov/pubmed/36826575 http://dx.doi.org/10.3390/jcdd10020079 |
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author | Wu, Jiahe Luo, Jingyi Cai, Huanhuan Li, Chenze Lei, Zhe Lu, Yi Ni, Lihua Cao, Jianlei Cheng, Bo Hu, Xiaorong |
author_facet | Wu, Jiahe Luo, Jingyi Cai, Huanhuan Li, Chenze Lei, Zhe Lu, Yi Ni, Lihua Cao, Jianlei Cheng, Bo Hu, Xiaorong |
author_sort | Wu, Jiahe |
collection | PubMed |
description | (1) Background: The molecular mechanism of oxidative stress-related genes (OSRGs) in myocardial ischemia–reperfusion injury (MIRI) has not been fully elucidated. (2) Methods: Differential expression analysis, enrichment analysis, and PPI analysis were performed on the MIRI-related datasets GSE160516 and GSE61592 to find key pathways and hub genes. OSRGs were obtained from the Molecular Signatures Database (MSigDB). The expression pattern and time changes of them were studied on the basis of their raw expression data. Corresponding online databases were used to predict miRNAs, transcription factors (TFs), and therapeutic drugs targeting common differentially expressed OSRGs. These identified OSRGs were further verified in the external dataset GSE4105 and H9C2 cell hypoxia–reoxygenation (HR) model. (3) Results: A total of 134 DEGs of MIRI were identified which were enriched in the pathways of “immune response”, “inflammatory response”, “neutrophil chemotaxis”, “phagosome”, and “platelet activation”. Six hub genes and 12 common differentially expressed OSRGs were identified. A total of 168 miRNAs, 41 TFs, and 21 therapeutic drugs were predicted targeting these OSRGs. Lastly, the expression trends of Aif1, Apoe, Arg1, Col1a1, Gpx7, and Hmox1 were confirmed in the external dataset and HR model. (4) Conclusions: Aif1, Apoe, Arg1, Col1a1, Gpx7, and Hmox1 may be involved in the oxidative stress mechanism of MIRI, and the intervention of these genes may be a potential therapeutic strategy. |
format | Online Article Text |
id | pubmed-9961140 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-99611402023-02-26 Expression Pattern and Molecular Mechanism of Oxidative Stress-Related Genes in Myocardial Ischemia–Reperfusion Injury Wu, Jiahe Luo, Jingyi Cai, Huanhuan Li, Chenze Lei, Zhe Lu, Yi Ni, Lihua Cao, Jianlei Cheng, Bo Hu, Xiaorong J Cardiovasc Dev Dis Article (1) Background: The molecular mechanism of oxidative stress-related genes (OSRGs) in myocardial ischemia–reperfusion injury (MIRI) has not been fully elucidated. (2) Methods: Differential expression analysis, enrichment analysis, and PPI analysis were performed on the MIRI-related datasets GSE160516 and GSE61592 to find key pathways and hub genes. OSRGs were obtained from the Molecular Signatures Database (MSigDB). The expression pattern and time changes of them were studied on the basis of their raw expression data. Corresponding online databases were used to predict miRNAs, transcription factors (TFs), and therapeutic drugs targeting common differentially expressed OSRGs. These identified OSRGs were further verified in the external dataset GSE4105 and H9C2 cell hypoxia–reoxygenation (HR) model. (3) Results: A total of 134 DEGs of MIRI were identified which were enriched in the pathways of “immune response”, “inflammatory response”, “neutrophil chemotaxis”, “phagosome”, and “platelet activation”. Six hub genes and 12 common differentially expressed OSRGs were identified. A total of 168 miRNAs, 41 TFs, and 21 therapeutic drugs were predicted targeting these OSRGs. Lastly, the expression trends of Aif1, Apoe, Arg1, Col1a1, Gpx7, and Hmox1 were confirmed in the external dataset and HR model. (4) Conclusions: Aif1, Apoe, Arg1, Col1a1, Gpx7, and Hmox1 may be involved in the oxidative stress mechanism of MIRI, and the intervention of these genes may be a potential therapeutic strategy. MDPI 2023-02-13 /pmc/articles/PMC9961140/ /pubmed/36826575 http://dx.doi.org/10.3390/jcdd10020079 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Wu, Jiahe Luo, Jingyi Cai, Huanhuan Li, Chenze Lei, Zhe Lu, Yi Ni, Lihua Cao, Jianlei Cheng, Bo Hu, Xiaorong Expression Pattern and Molecular Mechanism of Oxidative Stress-Related Genes in Myocardial Ischemia–Reperfusion Injury |
title | Expression Pattern and Molecular Mechanism of Oxidative Stress-Related Genes in Myocardial Ischemia–Reperfusion Injury |
title_full | Expression Pattern and Molecular Mechanism of Oxidative Stress-Related Genes in Myocardial Ischemia–Reperfusion Injury |
title_fullStr | Expression Pattern and Molecular Mechanism of Oxidative Stress-Related Genes in Myocardial Ischemia–Reperfusion Injury |
title_full_unstemmed | Expression Pattern and Molecular Mechanism of Oxidative Stress-Related Genes in Myocardial Ischemia–Reperfusion Injury |
title_short | Expression Pattern and Molecular Mechanism of Oxidative Stress-Related Genes in Myocardial Ischemia–Reperfusion Injury |
title_sort | expression pattern and molecular mechanism of oxidative stress-related genes in myocardial ischemia–reperfusion injury |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9961140/ https://www.ncbi.nlm.nih.gov/pubmed/36826575 http://dx.doi.org/10.3390/jcdd10020079 |
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