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Identifying key genes for diabetic kidney disease by bioinformatics analysis
BACKGROUND: There are no reliable molecular targets for early diagnosis and effective treatment in the clinical management of diabetic kidney disease (DKD). To identify novel gene factors underlying the progression of DKD. METHODS: The public transcriptomic datasets of the alloxan-induced DKD model...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10585855/ https://www.ncbi.nlm.nih.gov/pubmed/37853335 http://dx.doi.org/10.1186/s12882-023-03362-4 |
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author | Xu, Yushan Li, Lan Tang, Ping Zhang, Jingrong Zhong, Ruxian Luo, Jingmei Lin, Jie Zhang, Lihua |
author_facet | Xu, Yushan Li, Lan Tang, Ping Zhang, Jingrong Zhong, Ruxian Luo, Jingmei Lin, Jie Zhang, Lihua |
author_sort | Xu, Yushan |
collection | PubMed |
description | BACKGROUND: There are no reliable molecular targets for early diagnosis and effective treatment in the clinical management of diabetic kidney disease (DKD). To identify novel gene factors underlying the progression of DKD. METHODS: The public transcriptomic datasets of the alloxan-induced DKD model and the streptozotocin-induced DKD model were retrieved to perform an integrative bioinformatic analysis of differentially expressed genes (DEGs) shared by two experimental animal models. The dominant biological processes and pathways associated with DEGs were identified through enrichment analysis. The expression changes of the key DEGs were validated in the classic db/db DKD mouse model. RESULTS: The downregulated and upregulated genes in DKD models were uncovered from GSE139317 and GSE131221 microarray datasets. Enrichment analysis revealed that metabolic process, extracellular exosomes, and hydrolase activity are shared biological processes and molecular activity is altered in the DEGs. Importantly, Hmgcs2, angptl4, and Slco1a1 displayed a consistent expression pattern across the two DKD models. In the classic db/db DKD mice, Hmgcs2 and angptl4 were also found to be upregulated while Slco1a1 was downregulated in comparison to the control animals. CONCLUSIONS: In summary, we identified the common biological processes and molecular activity being altered in two DKD experimental models, as well as the novel gene factors (Hmgcs2, Angptl4, and Slco1a1) which may be implicated in DKD. Future works are warranted to decipher the biological role of these genes in the pathogenesis of DKD. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12882-023-03362-4. |
format | Online Article Text |
id | pubmed-10585855 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-105858552023-10-20 Identifying key genes for diabetic kidney disease by bioinformatics analysis Xu, Yushan Li, Lan Tang, Ping Zhang, Jingrong Zhong, Ruxian Luo, Jingmei Lin, Jie Zhang, Lihua BMC Nephrol Research BACKGROUND: There are no reliable molecular targets for early diagnosis and effective treatment in the clinical management of diabetic kidney disease (DKD). To identify novel gene factors underlying the progression of DKD. METHODS: The public transcriptomic datasets of the alloxan-induced DKD model and the streptozotocin-induced DKD model were retrieved to perform an integrative bioinformatic analysis of differentially expressed genes (DEGs) shared by two experimental animal models. The dominant biological processes and pathways associated with DEGs were identified through enrichment analysis. The expression changes of the key DEGs were validated in the classic db/db DKD mouse model. RESULTS: The downregulated and upregulated genes in DKD models were uncovered from GSE139317 and GSE131221 microarray datasets. Enrichment analysis revealed that metabolic process, extracellular exosomes, and hydrolase activity are shared biological processes and molecular activity is altered in the DEGs. Importantly, Hmgcs2, angptl4, and Slco1a1 displayed a consistent expression pattern across the two DKD models. In the classic db/db DKD mice, Hmgcs2 and angptl4 were also found to be upregulated while Slco1a1 was downregulated in comparison to the control animals. CONCLUSIONS: In summary, we identified the common biological processes and molecular activity being altered in two DKD experimental models, as well as the novel gene factors (Hmgcs2, Angptl4, and Slco1a1) which may be implicated in DKD. Future works are warranted to decipher the biological role of these genes in the pathogenesis of DKD. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12882-023-03362-4. BioMed Central 2023-10-18 /pmc/articles/PMC10585855/ /pubmed/37853335 http://dx.doi.org/10.1186/s12882-023-03362-4 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/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Xu, Yushan Li, Lan Tang, Ping Zhang, Jingrong Zhong, Ruxian Luo, Jingmei Lin, Jie Zhang, Lihua Identifying key genes for diabetic kidney disease by bioinformatics analysis |
title | Identifying key genes for diabetic kidney disease by bioinformatics analysis |
title_full | Identifying key genes for diabetic kidney disease by bioinformatics analysis |
title_fullStr | Identifying key genes for diabetic kidney disease by bioinformatics analysis |
title_full_unstemmed | Identifying key genes for diabetic kidney disease by bioinformatics analysis |
title_short | Identifying key genes for diabetic kidney disease by bioinformatics analysis |
title_sort | identifying key genes for diabetic kidney disease by bioinformatics analysis |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10585855/ https://www.ncbi.nlm.nih.gov/pubmed/37853335 http://dx.doi.org/10.1186/s12882-023-03362-4 |
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