CCND1 Overexpression in Idiopathic Dilated Cardiomyopathy: A Promising Biomarker?

Genes (Basel). 2023 Jun 10;14(6):1243. doi: 10.3390/genes14061243.

Abstract

Cardiomyopathy, a disorder of electrical or heart muscle function, represents a type of cardiac muscle failure and culminates in severe heart conditions. The prevalence of dilated cardiomyopathy (DCM) is higher than that of other types (hypertrophic cardiomyopathy and restrictive cardiomyopathy) and causes many deaths. Idiopathic dilated cardiomyopathy (IDCM) is a type of DCM with an unknown underlying cause. This study aims to analyze the gene network of IDCM patients to identify disease biomarkers. Data were first extracted from the Gene Expression Omnibus (GEO) dataset and normalized based on the RMA algorithm (Bioconductor package), and differentially expressed genes were identified. The gene network was mapped on the STRING website, and the data were transferred to Cytoscape software to determine the top 100 genes. In the following, several genes, including VEGFA, IGF1, APP, STAT1, CCND1, MYH10, and MYH11, were selected for clinical studies. Peripheral blood samples were taken from 14 identified IDCM patients and 14 controls. The RT-PCR results revealed no significant differences in the expression of the genes APP, MYH10, and MYH11 between the two groups. By contrast, the STAT1, IGF1, CCND1, and VEGFA genes were overexpressed in patients more than in controls. The highest expression was found for VEGFA, followed by CCND1 (p < 0.001). Overexpression of these genes may contribute to disease progression in patients with IDCM. However, more patients and genes need to be analyzed in order to achieve more robust results.

Keywords: DisGeNET; bioinformatics; diabetes; gene network analysis; microRNA.

MeSH terms

  • Biomarkers
  • Cardiomyopathies* / genetics
  • Cardiomyopathy, Dilated* / genetics
  • Cyclin D1
  • Heart Failure*
  • Humans
  • Myocardium

Substances

  • Biomarkers
  • CCND1 protein, human
  • Cyclin D1

Grants and funding

This research received no external funding.