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Investigation into the underlying molecular mechanisms of hypertensive nephrosclerosis using bioinformatics analyses

Hypertensive nephrosclerosis (HNS) is a major risk factor for end-stage renal disease. However, the underlying pathogenesis of HNS remains to be fully determined. The gene expression profile of GSE20602, which consists of 14 glomeruli samples from patients with HNS and 4 normal glomeruli control sam...

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Autores principales: Liu, Tianlong, Liu, Minna, Shang, Peijin, Jin, Xin, Liu, Wenxing, Zhang, Yikai, Li, Xinfang, Ding, Yi, Li, Yuwen, Wen, Aidong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5802219/
https://www.ncbi.nlm.nih.gov/pubmed/29328390
http://dx.doi.org/10.3892/mmr.2018.8405
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author Liu, Tianlong
Liu, Minna
Shang, Peijin
Jin, Xin
Liu, Wenxing
Zhang, Yikai
Li, Xinfang
Ding, Yi
Li, Yuwen
Wen, Aidong
author_facet Liu, Tianlong
Liu, Minna
Shang, Peijin
Jin, Xin
Liu, Wenxing
Zhang, Yikai
Li, Xinfang
Ding, Yi
Li, Yuwen
Wen, Aidong
author_sort Liu, Tianlong
collection PubMed
description Hypertensive nephrosclerosis (HNS) is a major risk factor for end-stage renal disease. However, the underlying pathogenesis of HNS remains to be fully determined. The gene expression profile of GSE20602, which consists of 14 glomeruli samples from patients with HNS and 4 normal glomeruli control samples, was obtained from the Gene Expression Omnibus database. Gene ontology (GO) and pathway enrichment analyses were performed in order to investigate the functions and pathways of differentially expressed genes (DEGs). Pathway relation and co-expression networks were constructed in order to identify key genes and signaling pathways involved in HNS. In total, 483 DEGs were identified to be associated with HNS, including 302 upregulated genes and 181 downregulated genes. Furthermore, GO analysis revealed that DEGs were significantly enriched in the small molecule metabolic process. In addition, pathway analysis also revealed that DEGs were predominantly involved in metabolic pathways. The tricarboxylic acid (TCA) cycle was identified as the hub pathway in the pathway relation network, whereas the sorbitol dehydrogenase (SORD) and cubulin (CUBN) genes were revealed to be the hub genes in the co-expression network. The present study revealed that the SORD, CUBN and albumin genes as well as the TCA cycle and metabolic pathways are involved in the pathogenesis of HNS. The results of the present study may contribute to the determination of the molecular mechanisms underlying HNS, and provide insight into the exploration of novel targets for the diagnosis and treatment of HNS.
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spelling pubmed-58022192018-02-26 Investigation into the underlying molecular mechanisms of hypertensive nephrosclerosis using bioinformatics analyses Liu, Tianlong Liu, Minna Shang, Peijin Jin, Xin Liu, Wenxing Zhang, Yikai Li, Xinfang Ding, Yi Li, Yuwen Wen, Aidong Mol Med Rep Articles Hypertensive nephrosclerosis (HNS) is a major risk factor for end-stage renal disease. However, the underlying pathogenesis of HNS remains to be fully determined. The gene expression profile of GSE20602, which consists of 14 glomeruli samples from patients with HNS and 4 normal glomeruli control samples, was obtained from the Gene Expression Omnibus database. Gene ontology (GO) and pathway enrichment analyses were performed in order to investigate the functions and pathways of differentially expressed genes (DEGs). Pathway relation and co-expression networks were constructed in order to identify key genes and signaling pathways involved in HNS. In total, 483 DEGs were identified to be associated with HNS, including 302 upregulated genes and 181 downregulated genes. Furthermore, GO analysis revealed that DEGs were significantly enriched in the small molecule metabolic process. In addition, pathway analysis also revealed that DEGs were predominantly involved in metabolic pathways. The tricarboxylic acid (TCA) cycle was identified as the hub pathway in the pathway relation network, whereas the sorbitol dehydrogenase (SORD) and cubulin (CUBN) genes were revealed to be the hub genes in the co-expression network. The present study revealed that the SORD, CUBN and albumin genes as well as the TCA cycle and metabolic pathways are involved in the pathogenesis of HNS. The results of the present study may contribute to the determination of the molecular mechanisms underlying HNS, and provide insight into the exploration of novel targets for the diagnosis and treatment of HNS. D.A. Spandidos 2018-03 2018-01-09 /pmc/articles/PMC5802219/ /pubmed/29328390 http://dx.doi.org/10.3892/mmr.2018.8405 Text en Copyright: © Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Liu, Tianlong
Liu, Minna
Shang, Peijin
Jin, Xin
Liu, Wenxing
Zhang, Yikai
Li, Xinfang
Ding, Yi
Li, Yuwen
Wen, Aidong
Investigation into the underlying molecular mechanisms of hypertensive nephrosclerosis using bioinformatics analyses
title Investigation into the underlying molecular mechanisms of hypertensive nephrosclerosis using bioinformatics analyses
title_full Investigation into the underlying molecular mechanisms of hypertensive nephrosclerosis using bioinformatics analyses
title_fullStr Investigation into the underlying molecular mechanisms of hypertensive nephrosclerosis using bioinformatics analyses
title_full_unstemmed Investigation into the underlying molecular mechanisms of hypertensive nephrosclerosis using bioinformatics analyses
title_short Investigation into the underlying molecular mechanisms of hypertensive nephrosclerosis using bioinformatics analyses
title_sort investigation into the underlying molecular mechanisms of hypertensive nephrosclerosis using bioinformatics analyses
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5802219/
https://www.ncbi.nlm.nih.gov/pubmed/29328390
http://dx.doi.org/10.3892/mmr.2018.8405
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