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Exploring the molecular mechanism underlying the psoriasis and T2D by using microarray data analysis
Although a large number of evidence has identified that psoriasis is significantly correlated with type 2 diabetes (T2D), the common molecular mechanism of its occurrence remains unclear. Our study aims to further elucidate the mechanism of the occurrence of this complication. We obtained the gene e...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10630520/ https://www.ncbi.nlm.nih.gov/pubmed/37935955 http://dx.doi.org/10.1038/s41598-023-46795-5 |
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author | Yang, Li Zhang, Lei Du, Qingfang Gong, Xiaoyu Tian, Jun |
author_facet | Yang, Li Zhang, Lei Du, Qingfang Gong, Xiaoyu Tian, Jun |
author_sort | Yang, Li |
collection | PubMed |
description | Although a large number of evidence has identified that psoriasis is significantly correlated with type 2 diabetes (T2D), the common molecular mechanism of its occurrence remains unclear. Our study aims to further elucidate the mechanism of the occurrence of this complication. We obtained the gene expression data of psoriasis (GSE30999) and T2D (GSE28829) from the Gene Expression Omnibus (GEO) dataset. Then the common differentially expressed genes (DEGs) of T2D and psoriasis were identified. After that, we performed three types of analyses about these DEGs, including functional enrichment analysis, protein–protein interaction (PPI) network and module manufacture, hub genes identification and co-expression analysis. 132 common DEGs (14 upregulated genes and 118 downregulated genes) were identified for subsequent a series of analyses. Function enrichment analysis demonstrated that Rap1 signaling pathway, PI3K-Akt signaling pathway, and cGMP-PKG signaling pathway may play a significant role in pathogenesis of psoriasis and T2D. Finally, 3 important hub genes were selected by utilizing cytoHubba, including SNRPN, GNAS, IGF2. Our work reveals the potential common signaling pathways of psoriasis and T2D. These Hub genes and common signaling pathways provide insights for further investigation of molecular mechanism about psoriasis and T2D. |
format | Online Article Text |
id | pubmed-10630520 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-106305202023-11-07 Exploring the molecular mechanism underlying the psoriasis and T2D by using microarray data analysis Yang, Li Zhang, Lei Du, Qingfang Gong, Xiaoyu Tian, Jun Sci Rep Article Although a large number of evidence has identified that psoriasis is significantly correlated with type 2 diabetes (T2D), the common molecular mechanism of its occurrence remains unclear. Our study aims to further elucidate the mechanism of the occurrence of this complication. We obtained the gene expression data of psoriasis (GSE30999) and T2D (GSE28829) from the Gene Expression Omnibus (GEO) dataset. Then the common differentially expressed genes (DEGs) of T2D and psoriasis were identified. After that, we performed three types of analyses about these DEGs, including functional enrichment analysis, protein–protein interaction (PPI) network and module manufacture, hub genes identification and co-expression analysis. 132 common DEGs (14 upregulated genes and 118 downregulated genes) were identified for subsequent a series of analyses. Function enrichment analysis demonstrated that Rap1 signaling pathway, PI3K-Akt signaling pathway, and cGMP-PKG signaling pathway may play a significant role in pathogenesis of psoriasis and T2D. Finally, 3 important hub genes were selected by utilizing cytoHubba, including SNRPN, GNAS, IGF2. Our work reveals the potential common signaling pathways of psoriasis and T2D. These Hub genes and common signaling pathways provide insights for further investigation of molecular mechanism about psoriasis and T2D. Nature Publishing Group UK 2023-11-07 /pmc/articles/PMC10630520/ /pubmed/37935955 http://dx.doi.org/10.1038/s41598-023-46795-5 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Yang, Li Zhang, Lei Du, Qingfang Gong, Xiaoyu Tian, Jun Exploring the molecular mechanism underlying the psoriasis and T2D by using microarray data analysis |
title | Exploring the molecular mechanism underlying the psoriasis and T2D by using microarray data analysis |
title_full | Exploring the molecular mechanism underlying the psoriasis and T2D by using microarray data analysis |
title_fullStr | Exploring the molecular mechanism underlying the psoriasis and T2D by using microarray data analysis |
title_full_unstemmed | Exploring the molecular mechanism underlying the psoriasis and T2D by using microarray data analysis |
title_short | Exploring the molecular mechanism underlying the psoriasis and T2D by using microarray data analysis |
title_sort | exploring the molecular mechanism underlying the psoriasis and t2d by using microarray data analysis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10630520/ https://www.ncbi.nlm.nih.gov/pubmed/37935955 http://dx.doi.org/10.1038/s41598-023-46795-5 |
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