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Molecular Signatures of Human Chronic Atrial Fibrillation in Primary Mitral Regurgitation

Günseli Çubukçuoğlu Deniz1,2, Serkan Durdu2,3, Yeşim Doğan2

  • 1Stem Cell Institute, Ankara University, Ankara, Turkey.

Cardiovascular Therapeutics
|November 5, 2021
PubMed
Abstract

Insights

Atrial fibrillation (AFib) in mitral regurgitation (MR) shows distinct gene expression changes, including pathways for heart failure and structural remodeling. These molecular alterations in AFib may reveal new therapeutic targets for patients.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Genomics

Background:

  • Atrial fibrillation (AFib) in chronic primary mitral regurgitation (MR) lacks detailed transcriptomic characterization.
  • Understanding AFib pathophysiology in MR is crucial for developing targeted therapies.

Purpose of the Study:

  • To compare gene expression profiles in patients with degenerative MR experiencing AFib versus sinus rhythm (SR).
  • To elucidate the molecular mechanisms underlying AFib in the context of primary MR.

Main Methods:

  • Transcriptomic analysis and bioinformatics on 59 patients.
  • Differential gene expression analysis with a 1.5-fold change threshold.
  • Meta-analysis using independent datasets from the Gene Expression Omnibus (GEO).

Main Results:

  • AFib persistence correlated with increased expression of genes linked to heart failure (NPPB, ANGPTL2, IGFBP2), structural remodeling (COLQ, COMP, DHRS9, CHGB), and cellular stress (DNAJA4).
  • Decreased expression of genes involved in structural (BMP7) and electrical remodeling (CACNB2, MCOLN3) was observed in AFib atria.
  • Transmission electron microscopy confirmed ultrastructural atrial remodeling and autophagy in AFib samples.

Conclusions:

  • Persistent AFib in primary MR is associated with significant alterations in atrial cardiomyocyte gene expression compared to SR.
  • These gene expression changes highlight potential novel therapeutic targets for AFib management in MR patients.

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