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Identifying critical genes and pathways of doxorubicin-induced cardiomyopathy via bioinformatics analysis

G Fan1, X Shi, C Huo

  • 1Cardiology Department, Xianyang Central Hospital, Xianyang, Shaanxi Province, China. nfgcardiology@126.com.

European Review for Medical and Pharmacological Sciences
|March 18, 2024
PubMed
Abstract

Insights

This study identifies key genes and pathways in doxorubicin-induced cardiomyopathy (DCM) using bioinformatics. Findings may reveal novel therapeutic targets for this heart condition.

Area of Science:

  • Cardiovascular Biology
  • Genomics
  • Bioinformatics

Background:

  • Doxorubicin (DOX) can cause heart damage, known as doxorubicin-induced cardiomyopathy (DCM).
  • The exact biological mechanisms driving DCM are not fully understood.
  • Identifying critical genes and pathways is crucial for understanding and treating DCM.

Purpose of the Study:

  • To pinpoint key genes and molecular pathways implicated in doxorubicin-induced cardiomyopathy (DCM).
  • To leverage bioinformatics analysis for novel insights into DCM pathogenesis.
  • To identify potential therapeutic targets for DCM.

Main Methods:

  • Utilized Gene Expression Omnibus (GEO) datasets (GSE59672, GSE23598) of mouse heart tissue.
  • Applied R software (limma, clusterProfiler) for differential gene expression (DEG) analysis, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis.
  • Constructed Protein-Protein Interaction (PPI) networks using STRING and Cytoscape (cytoHubba) to identify hub genes.

Main Results:

  • Identified 492 and 501 DEGs in the two datasets.
  • GO analysis highlighted roles in extracellular matrix organization and metabolic processes.
  • KEGG analysis revealed involvement in ECM-receptor interaction and p53 signaling pathways.
  • Eight hub genes were identified: Col1a1, Col3a1, Col1a2, Col6a1, Ptprc, Tyrobp, Itgb2, and Ctss.

Conclusions:

  • Identified critical genes (Col1a1, Col3a1, Col1a2, Col6a1, Ptprc, Tyrobp, Itgb2, Ctss) in DCM.
  • Discovered significant molecular pathways contributing to DCM pathogenesis.
  • Results offer potential novel molecular mechanisms and therapeutic targets for DCM.

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