Open Access

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

  • Authors:
    • Tianlong Liu
    • Minna Liu
    • Peijin Shang
    • Xin Jin
    • Wenxing Liu
    • Yikai Zhang
    • Xinfang Li
    • Yi Ding
    • Yuwen Li
    • Aidong Wen
  • View Affiliations

  • Published online on: January 9, 2018     https://doi.org/10.3892/mmr.2018.8405
  • Pages: 4440-4448
  • Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

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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March-2018
Volume 17 Issue 3

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Liu T, Liu M, Shang P, Jin X, Liu W, Zhang Y, Li X, Ding Y, Li Y, Wen A, Wen A, et al: Investigation into the underlying molecular mechanisms of hypertensive nephrosclerosis using bioinformatics analyses. Mol Med Rep 17: 4440-4448, 2018.
APA
Liu, T., Liu, M., Shang, P., Jin, X., Liu, W., Zhang, Y. ... Wen, A. (2018). Investigation into the underlying molecular mechanisms of hypertensive nephrosclerosis using bioinformatics analyses. Molecular Medicine Reports, 17, 4440-4448. https://doi.org/10.3892/mmr.2018.8405
MLA
Liu, T., Liu, M., Shang, P., Jin, X., Liu, W., Zhang, Y., Li, X., Ding, Y., Li, Y., Wen, A."Investigation into the underlying molecular mechanisms of hypertensive nephrosclerosis using bioinformatics analyses". Molecular Medicine Reports 17.3 (2018): 4440-4448.
Chicago
Liu, T., Liu, M., Shang, P., Jin, X., Liu, W., Zhang, Y., Li, X., Ding, Y., Li, Y., Wen, A."Investigation into the underlying molecular mechanisms of hypertensive nephrosclerosis using bioinformatics analyses". Molecular Medicine Reports 17, no. 3 (2018): 4440-4448. https://doi.org/10.3892/mmr.2018.8405