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Identification of the molecular mechanism and candidate markers for diabetic nephropathy
BACKGROUND: Diabetic nephropathy (DN) is one of the most common complications in diabetic patients. New strategies are needed to delay the occurrence and development of this pathology. METHODS: Differentially expressed genes (DEGs) in glomeruli and renal tubules were identified using the GSE30122 da...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
AME Publishing Company
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9761143/ https://www.ncbi.nlm.nih.gov/pubmed/36544633 http://dx.doi.org/10.21037/atm-22-5128 |
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author | Chen, Chun Liu, Liping Luo, Jia |
author_facet | Chen, Chun Liu, Liping Luo, Jia |
author_sort | Chen, Chun |
collection | PubMed |
description | BACKGROUND: Diabetic nephropathy (DN) is one of the most common complications in diabetic patients. New strategies are needed to delay the occurrence and development of this pathology. METHODS: Differentially expressed genes (DEGs) in glomeruli and renal tubules were identified using the GSE30122 dataset, and a co-expression network was constructed to identify the hub genes of modules. The biological function and signaling pathway of the module genes were also analyzed. In addition, the expression of 24 immune cells and the area under the receiver operating characteristic (ROC) curve (AUC) values of the hub genes were also calculated. RESULTS: A total of 1,778 DEGs were isolated from glomeruli and 1,996 DEGs were isolated from renal tubules. Nine modules and their hub genes were identified using the co-expression network. Enrichment analysis showed that the module genes were mainly enriched in immune inflammation and oxidative stress. The expressions of B cells, activated dendritic cell, and T cells in the glomeruli and renal tubules of DN patients were higher than those in the controls, and the correlation between these immune cells was the strongest. Collagen type I alpha 2 chain (COL1A2), the hub gene of the brown module, had the highest AUC values and may have a better clinical diagnostic ability. CONCLUSIONS: In conclusion, the module genes and related biological functions and signaling pathways found in this study can deepen our understanding of the molecular mechanism of DN progression. COL1A2 may be a potential biomarker for DN. |
format | Online Article Text |
id | pubmed-9761143 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | AME Publishing Company |
record_format | MEDLINE/PubMed |
spelling | pubmed-97611432022-12-20 Identification of the molecular mechanism and candidate markers for diabetic nephropathy Chen, Chun Liu, Liping Luo, Jia Ann Transl Med Original Article BACKGROUND: Diabetic nephropathy (DN) is one of the most common complications in diabetic patients. New strategies are needed to delay the occurrence and development of this pathology. METHODS: Differentially expressed genes (DEGs) in glomeruli and renal tubules were identified using the GSE30122 dataset, and a co-expression network was constructed to identify the hub genes of modules. The biological function and signaling pathway of the module genes were also analyzed. In addition, the expression of 24 immune cells and the area under the receiver operating characteristic (ROC) curve (AUC) values of the hub genes were also calculated. RESULTS: A total of 1,778 DEGs were isolated from glomeruli and 1,996 DEGs were isolated from renal tubules. Nine modules and their hub genes were identified using the co-expression network. Enrichment analysis showed that the module genes were mainly enriched in immune inflammation and oxidative stress. The expressions of B cells, activated dendritic cell, and T cells in the glomeruli and renal tubules of DN patients were higher than those in the controls, and the correlation between these immune cells was the strongest. Collagen type I alpha 2 chain (COL1A2), the hub gene of the brown module, had the highest AUC values and may have a better clinical diagnostic ability. CONCLUSIONS: In conclusion, the module genes and related biological functions and signaling pathways found in this study can deepen our understanding of the molecular mechanism of DN progression. COL1A2 may be a potential biomarker for DN. AME Publishing Company 2022-11 /pmc/articles/PMC9761143/ /pubmed/36544633 http://dx.doi.org/10.21037/atm-22-5128 Text en 2022 Annals of Translational Medicine. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) . |
spellingShingle | Original Article Chen, Chun Liu, Liping Luo, Jia Identification of the molecular mechanism and candidate markers for diabetic nephropathy |
title | Identification of the molecular mechanism and candidate markers for diabetic nephropathy |
title_full | Identification of the molecular mechanism and candidate markers for diabetic nephropathy |
title_fullStr | Identification of the molecular mechanism and candidate markers for diabetic nephropathy |
title_full_unstemmed | Identification of the molecular mechanism and candidate markers for diabetic nephropathy |
title_short | Identification of the molecular mechanism and candidate markers for diabetic nephropathy |
title_sort | identification of the molecular mechanism and candidate markers for diabetic nephropathy |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9761143/ https://www.ncbi.nlm.nih.gov/pubmed/36544633 http://dx.doi.org/10.21037/atm-22-5128 |
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