Computational Analysis Reveals Distinctive Interaction of miRNAs with Target Genes in the Pathogenesis of Chronic Kidney Disease

Genes (Basel). 2023 Apr 12;14(4):898. doi: 10.3390/genes14040898.

Abstract

The regulation of genes is crucial for maintaining a healthy intracellular environment, and any dysregulation of gene expression leads to several pathological complications. It is known that many diseases, including kidney diseases, are regulated by miRNAs. However, the data on the use of miRNAs as biomarkers for the diagnosis and treatment of chronic kidney disease (CKD) are not conclusive. The purpose of this study was to elucidate the potential of miRNAs as an efficient biomarker for the detection and treatment of CKD at its early stages. Gene expression profiling data were acquired from the Gene Expression Omnibus (GEO) and differentially expressed genes (DEGs) were identified. miRNAs directly associated with CKD were obtained from an extensive literature search. Network illustration of miRNAs and their projected target differentially expressed genes (tDEGs) was accomplished, followed by functional enrichment analysis. hsa-miR-1-3p, hsa-miR-206, hsa-miR-494 and hsa-miR-577 exhibited a strong association with CKD through the regulation of genes involved in signal transduction, cell proliferation, the regulation of transcription and apoptotic process. All these miRNAs have shown significant contributions to the inflammatory response and the processes which eventually lead to the pathogenesis of CKD. The in silico approach used in this research represents a comprehensive analysis of identified miRNAs and their target genes for the identification of molecular markers of disease processes. The outcomes of the study recommend further efforts for developing miRNA biomarkers set for the early diagnosis of CKD.

Keywords: biomarker; chronic kidney disease; gene expression; miRNA; pathogenesis.

MeSH terms

  • Gene Expression Profiling
  • Humans
  • MicroRNAs* / metabolism
  • Microarray Analysis
  • Renal Insufficiency, Chronic* / genetics
  • Signal Transduction / genetics

Substances

  • MicroRNAs
  • MIRN206 microRNA, human
  • MIRN577 microRNA, human

Grants and funding

This research received no external funding.