4.6 Article

Comprehensive Bioinformatics Analysis Identifies POLR2I as a Key Gene in the Pathogenesis of Hypertensive Nephropathy

Journal

FRONTIERS IN GENETICS
Volume 12, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fgene.2021.698570

Keywords

hypertensive nephropathy (HN); weighted gene co-expression network analysis (WGCNA); differentially expressed genes (DEGs); pathogenesis; key gene; POLR2I

Funding

  1. National Natural Science Foundation of China [81900372, 81970211, 81900355, 81800361]
  2. Doctoral Start-up Foundation of Liaoning Province [20180540113]
  3. National Key Research and Development Program of China [2017YFC1307600]
  4. Department of Science and Technology of Liaoning Province, China [2020JH1/10300002]
  5. post-doctoral innovative talents support program [BX2021376]

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This study identified POLR2I as a key gene related to the pathogenesis of hypertensive nephropathy, providing new insights into the molecular mechanisms underlying this disease.
Hypertensive nephropathy (HN), mainly caused by chronic hypertension, is one of the major causes of end-stage renal disease. However, the pathogenesis of HN remains unclarified, and there is an urgent need for improved treatments. Gene expression profiles for HN and normal tissue were obtained from the Gene Expression Omnibus database. A total of 229 differentially co-expressed genes were identified by weighted gene co-expression network analysis and differential gene expression analysis. These genes were used to construct protein-protein interaction networks to search for hub genes. Following validation in an independent external dataset and in a clinical database, POLR2I, one of the hub genes, was identified as a key gene related to the pathogenesis of HN. The expression level of POLR2I is upregulated in HN, and the up-regulation of POLR2I is positively correlated with renal function in HN. Finally, we verified the protein levels of POLR2I in vivo to confirm the accuracy of our analysis. In conclusion, our study identified POLR2I as a key gene related to the pathogenesis of HN, providing new insights into the molecular mechanisms underlying HN.

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