Exploring the pathogenesis and immune infiltration in dilated cardiomyopathy complicated with atrial fibrillation by

Ting Gan1,2,3, Jing Hu4, Anwer Khalid Okab Aledan1,2,3

  • 1Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Frontiers in Immunology
|February 3, 2023
PubMed

Insights

Dilated cardiomyopathy (DCM) and atrial fibrillation (AF) share common immune dysregulation, particularly involving follicular helper T cells and CD48/CD3D genes. These findings suggest a potential shared pathogenesis and diagnostic markers for DCM with AF.

Area of Science:

  • Cardiology
  • Immunology
  • Bioinformatics

Background:

  • Atrial fibrillation (AF) is a serious complication of dilated cardiomyopathy (DCM), increasing risks for thromboembolic events and sudden death.
  • The underlying molecular mechanisms and immune infiltration patterns common to DCM and AF remain largely unelucidated.
  • This study aims to explore these shared mechanisms using comprehensive bioinformatics analysis.

Purpose of the Study:

  • To identify common molecular mechanisms between DCM and AF.
  • To analyze immune cell infiltration patterns in DCM complicated with AF.
  • To discover potential diagnostic biomarkers for DCM with AF.

Main Methods:

  • Utilized gene expression datasets for DCM and AF from the Gene Expression Omnibus database.
  • Performed differential gene expression analysis and constructed protein-protein interaction networks.
  • Employed ImmuCellAI for immune infiltration estimation and verified findings in validation datasets.

Main Results:

  • Identified 184 common differentially expressed genes (DEGs) between DCM and AF, with hub genes significantly associated with immune responses.
  • Discovered 7 hub immune-related genes (e.g., HLA-DRA, LCK, ITK, CD48, CD247, CD3D, IL2RG) and dysregulation of Monocyte, Neutrophil, and follicular helper T (Tfh) cells.
  • Found CD48 and CD3D demonstrated excellent diagnostic value for DCM and AF, correlating with Tfh cell abundance.

Conclusions:

  • Immune cell disorders, specifically Tfh cells, driven by hub immune-related genes like CD48 and CD3D, may represent a common pathogenic pathway in DCM combined with AF.
  • These findings provide a foundation for further research into the immune mechanisms underlying DCM and AF.
  • Identified CD48 and CD3D as potential diagnostic biomarkers for DCM with AF.
Abstract

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