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Exploring Key Genes and Pathways of Cardiac Hypertrophy Based on Bioinformatics

OBJECTIVE: This research is aimed at identifying the key genes and pathways of cardiac hypertrophy using bioinformatics and at providing a new target for the identification of cardiac hypertrophy. METHODS: Microarray data GSE1621 and GSE18801 were acquired from the GEO database. The DEGs of GSE1621...

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Autores principales: Zhang, Zhenzhen, Wang, Chunxiao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9423995/
https://www.ncbi.nlm.nih.gov/pubmed/36046382
http://dx.doi.org/10.1155/2022/2081590
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author Zhang, Zhenzhen
Wang, Chunxiao
author_facet Zhang, Zhenzhen
Wang, Chunxiao
author_sort Zhang, Zhenzhen
collection PubMed
description OBJECTIVE: This research is aimed at identifying the key genes and pathways of cardiac hypertrophy using bioinformatics and at providing a new target for the identification of cardiac hypertrophy. METHODS: Microarray data GSE1621 and GSE18801 were acquired from the GEO database. The DEGs of GSE1621 and GSE18801 were analyzed using the online tool GEO2R. “ggplot2” package of R software was utilized to generate the volcano plots. The top and bottom 10 genes were mapped as a heat map. GO functional annotation analysis and KEGG pathway enrichment analysis were performed separately for DEGs using the online software DAVID. Histograms were plotted using the R “ggplot2” package. The DEGs were imported into the STRING online database for constructing PPI networks and analyzing the DEG interaction relationships. RESULTS: In the present study, 469 DEGs were screened in GSE1621 and a total of 793 DEGs were screened in GSE18801. GO analyses indicate that DEGs were mainly involved in cardiac muscle contraction, regulation of blood circulation, regulation of muscle contraction, muscle contraction, striated muscle contraction, regulation of heart contraction, regulation of striated muscle contraction, and tissue remodeling. KEGG analyses indicate that DEGs were mainly involved in Th17 cell differentiation, Th1 and Th2 cell differentiation, HIF-1 signaling pathway, pathways in cancer, hematopoietic cell lineage, Chagas disease and cell adhesion molecules, viral myocarditis, central carbon metabolism in cancer, acute myeloid leukemia, and JAK-STAT signaling pathway. Eight hub genes were screened, including Akt1, Lox, Timp1, Col1al, Spp1, Ccnd1, Mmp3, and Egfr. CONCLUSIONS: The DEGs associated with cardiac hypertrophy were screened via bioinformatics analysis, and eight hub genes were identified, including Akt1, Lox, Timp1, Col1al, Spp1, Ccnd1, Mmp3, and Egfr, which might be a new target for the identification of cardiac hypertrophy.
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spelling pubmed-94239952022-08-30 Exploring Key Genes and Pathways of Cardiac Hypertrophy Based on Bioinformatics Zhang, Zhenzhen Wang, Chunxiao Dis Markers Research Article OBJECTIVE: This research is aimed at identifying the key genes and pathways of cardiac hypertrophy using bioinformatics and at providing a new target for the identification of cardiac hypertrophy. METHODS: Microarray data GSE1621 and GSE18801 were acquired from the GEO database. The DEGs of GSE1621 and GSE18801 were analyzed using the online tool GEO2R. “ggplot2” package of R software was utilized to generate the volcano plots. The top and bottom 10 genes were mapped as a heat map. GO functional annotation analysis and KEGG pathway enrichment analysis were performed separately for DEGs using the online software DAVID. Histograms were plotted using the R “ggplot2” package. The DEGs were imported into the STRING online database for constructing PPI networks and analyzing the DEG interaction relationships. RESULTS: In the present study, 469 DEGs were screened in GSE1621 and a total of 793 DEGs were screened in GSE18801. GO analyses indicate that DEGs were mainly involved in cardiac muscle contraction, regulation of blood circulation, regulation of muscle contraction, muscle contraction, striated muscle contraction, regulation of heart contraction, regulation of striated muscle contraction, and tissue remodeling. KEGG analyses indicate that DEGs were mainly involved in Th17 cell differentiation, Th1 and Th2 cell differentiation, HIF-1 signaling pathway, pathways in cancer, hematopoietic cell lineage, Chagas disease and cell adhesion molecules, viral myocarditis, central carbon metabolism in cancer, acute myeloid leukemia, and JAK-STAT signaling pathway. Eight hub genes were screened, including Akt1, Lox, Timp1, Col1al, Spp1, Ccnd1, Mmp3, and Egfr. CONCLUSIONS: The DEGs associated with cardiac hypertrophy were screened via bioinformatics analysis, and eight hub genes were identified, including Akt1, Lox, Timp1, Col1al, Spp1, Ccnd1, Mmp3, and Egfr, which might be a new target for the identification of cardiac hypertrophy. Hindawi 2022-08-22 /pmc/articles/PMC9423995/ /pubmed/36046382 http://dx.doi.org/10.1155/2022/2081590 Text en Copyright © 2022 Zhenzhen Zhang and Chunxiao Wang. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Zhang, Zhenzhen
Wang, Chunxiao
Exploring Key Genes and Pathways of Cardiac Hypertrophy Based on Bioinformatics
title Exploring Key Genes and Pathways of Cardiac Hypertrophy Based on Bioinformatics
title_full Exploring Key Genes and Pathways of Cardiac Hypertrophy Based on Bioinformatics
title_fullStr Exploring Key Genes and Pathways of Cardiac Hypertrophy Based on Bioinformatics
title_full_unstemmed Exploring Key Genes and Pathways of Cardiac Hypertrophy Based on Bioinformatics
title_short Exploring Key Genes and Pathways of Cardiac Hypertrophy Based on Bioinformatics
title_sort exploring key genes and pathways of cardiac hypertrophy based on bioinformatics
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9423995/
https://www.ncbi.nlm.nih.gov/pubmed/36046382
http://dx.doi.org/10.1155/2022/2081590
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