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Investigation of the shared molecular mechanisms and hub genes between myocardial infarction and depression

Mengxi Wang1,2,3, Liying Cheng4, Ziwei Gao1,2,3

  • 1Department of Cardiology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.

Frontiers in Cardiovascular Medicine
|August 7, 2023
PubMed

Insights

Bioinformatics identified shared immune inflammation pathways in myocardial infarction and depression. Six hub genes (CD24, CSTA, EXTL3, RPS7, SLC25A5, ZMAT3) show potential as biomarkers for diagnosing depression and identifying myocardial infarction subtypes.

Area of Science:

  • Genomics
  • Bioinformatics
  • Immunology

Background:

  • The shared pathogenesis between myocardial infarction and depression remains unclear.
  • Bioinformatics offers a powerful approach to investigate common disease mechanisms.

Purpose of the Study:

  • To identify shared differentially expressed genes (S-DEGs) between myocardial infarction and depression using bioinformatics.
  • To explore the underlying immune inflammatory mechanisms.
  • To identify potential diagnostic biomarkers and molecular subtypes.

Main Methods:

  • Differential gene expression analysis (M-DEGs, D-DEGs) and intersection to find S-DEGs.
  • Gene Ontology (GO), KEGG pathway, Gene Set Enrichment Analysis (GSEA), and Gene Set Variation Analysis (GSVA).
  • Machine learning for hub S-DEG identification, diagnostic model development, and molecular subtype clustering.

Main Results:

  • Six hub S-DEGs (CD24, CSTA, EXTL3, RPS7, SLC25A5, ZMAT3) involved in immune inflammatory response were identified.
  • Immune inflammation was confirmed as a shared pathogenesis.
  • The identified hub genes demonstrated diagnostic utility for depression and ability to distinguish myocardial infarction subtypes.

Conclusions:

  • Immune inflammation is a key shared pathway in myocardial infarction and depression.
  • The identified hub S-DEGs serve as promising biomarkers for disease diagnosis and molecular subtyping.
Abstract

Keywords:
depressiondiagnosisimmune inflammationmolecular subtypemyocardial infarctionpathogenesis

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