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Genetic analysis of potential biomarkers and therapeutic targets in ferroptosis from coronary artery disease
Ferroptosis plays a key role in the death of cells including cardiomyocytes, and it is related to a variety of cardiac diseases. However, the role of ferroptosis‐related genes (FRGs) in coronary artery disease (CAD) is not well characterized. We downloaded CAD‐related information and FRGs from the g...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8995456/ https://www.ncbi.nlm.nih.gov/pubmed/35152560 http://dx.doi.org/10.1111/jcmm.17239 |
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author | Wu, Xun Qin, Kele Iroegbu, Chukwuemeka Daniel Xiang, Kun Peng, Jun Guo, Jianjun Yang, Jinfu Fan, Chengming |
author_facet | Wu, Xun Qin, Kele Iroegbu, Chukwuemeka Daniel Xiang, Kun Peng, Jun Guo, Jianjun Yang, Jinfu Fan, Chengming |
author_sort | Wu, Xun |
collection | PubMed |
description | Ferroptosis plays a key role in the death of cells including cardiomyocytes, and it is related to a variety of cardiac diseases. However, the role of ferroptosis‐related genes (FRGs) in coronary artery disease (CAD) is not well characterized. We downloaded CAD‐related information and FRGs from the gene expression omnibus (GEO) database and Ferroptosis Database (FerrDb) respectively. A total of 10 CAD‐related DE‐FRGs were obtained, which were closely linked to autophagy regulation and immune response. Subsequently, CA9, CBS, CEBPG, HSPB1, SLC1A4, STMN1 and TRIB3 among the 10 DE‐FRGs were identified as marker genes by LASSO and SVM‐RFE algorithms, which had tolerable diagnostic capabilities. Subsequent functional enrichment analysis showed that these marker genes may play a corresponding role in CAD by participating in the regulation of immune response, amino acid metabolism, cell cycle and multiple pathways related to the pathogenesis of CAD. Furthermore, a total of 58 drugs targeting 7 marker genes had been obtained. On the contrary, the ceRNA network revealed a complex regulatory relationship based on the marker genes. Also, CIBERSORT analysis showed that the changes in the immune microenvironment of CAD patients may be related to CBS, HSPB1 and CEBPG. We developed a diagnostic potency and provided an insight for exploring the mechanism for CAD. Before clinical application, further research is needed to test its diagnostic value for CAD. |
format | Online Article Text |
id | pubmed-8995456 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-89954562022-04-15 Genetic analysis of potential biomarkers and therapeutic targets in ferroptosis from coronary artery disease Wu, Xun Qin, Kele Iroegbu, Chukwuemeka Daniel Xiang, Kun Peng, Jun Guo, Jianjun Yang, Jinfu Fan, Chengming J Cell Mol Med Original Articles Ferroptosis plays a key role in the death of cells including cardiomyocytes, and it is related to a variety of cardiac diseases. However, the role of ferroptosis‐related genes (FRGs) in coronary artery disease (CAD) is not well characterized. We downloaded CAD‐related information and FRGs from the gene expression omnibus (GEO) database and Ferroptosis Database (FerrDb) respectively. A total of 10 CAD‐related DE‐FRGs were obtained, which were closely linked to autophagy regulation and immune response. Subsequently, CA9, CBS, CEBPG, HSPB1, SLC1A4, STMN1 and TRIB3 among the 10 DE‐FRGs were identified as marker genes by LASSO and SVM‐RFE algorithms, which had tolerable diagnostic capabilities. Subsequent functional enrichment analysis showed that these marker genes may play a corresponding role in CAD by participating in the regulation of immune response, amino acid metabolism, cell cycle and multiple pathways related to the pathogenesis of CAD. Furthermore, a total of 58 drugs targeting 7 marker genes had been obtained. On the contrary, the ceRNA network revealed a complex regulatory relationship based on the marker genes. Also, CIBERSORT analysis showed that the changes in the immune microenvironment of CAD patients may be related to CBS, HSPB1 and CEBPG. We developed a diagnostic potency and provided an insight for exploring the mechanism for CAD. Before clinical application, further research is needed to test its diagnostic value for CAD. John Wiley and Sons Inc. 2022-02-13 2022-04 /pmc/articles/PMC8995456/ /pubmed/35152560 http://dx.doi.org/10.1111/jcmm.17239 Text en © 2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Wu, Xun Qin, Kele Iroegbu, Chukwuemeka Daniel Xiang, Kun Peng, Jun Guo, Jianjun Yang, Jinfu Fan, Chengming Genetic analysis of potential biomarkers and therapeutic targets in ferroptosis from coronary artery disease |
title | Genetic analysis of potential biomarkers and therapeutic targets in ferroptosis from coronary artery disease |
title_full | Genetic analysis of potential biomarkers and therapeutic targets in ferroptosis from coronary artery disease |
title_fullStr | Genetic analysis of potential biomarkers and therapeutic targets in ferroptosis from coronary artery disease |
title_full_unstemmed | Genetic analysis of potential biomarkers and therapeutic targets in ferroptosis from coronary artery disease |
title_short | Genetic analysis of potential biomarkers and therapeutic targets in ferroptosis from coronary artery disease |
title_sort | genetic analysis of potential biomarkers and therapeutic targets in ferroptosis from coronary artery disease |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8995456/ https://www.ncbi.nlm.nih.gov/pubmed/35152560 http://dx.doi.org/10.1111/jcmm.17239 |
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