Objective: Investigating the Role of Epicardial Adipose Tissue as a Catalyst for Reversal and Reconstruction of Atrial Myocardial Cells in the Context of Dialogue with Atrial Myocardial Cells. Implications for Breakthroughs in Preventing Paroxysmal Atrial Fibrillation Progression.
Methods: We obtained three datasets (GSE41177, GSE31821, and GSE135455) associated with atrial fibrillation (AF) from the Gene Expression Omnibus (GEO) database, which were subsequently merged for comprehensive analysis. Differentially expressed genes (DEGs) were identified using the "limma" package in the R software. Candidate AF genes were selected through machine learning techniques, including the LASSO regression algorithm and SVM-RFE algorithm. The diagnostic efficacy of these genes was evaluated using Receiver Operating Characteristic (ROC) curves. Additionally, CIBERSORT was employed to investigate the proportions of infiltrating immune cells in each sample, while the Pearson method was applied to examine the correlation between genes and immune cells. Further validation of the DEGs were performed by PCR in atrial fibrillation rats.
Results: A total of 310 Differentially Expressed Genes (DEGs) were identified in atrial cardiomyocytes with epicardial adipose tissue. Using the LASSO regression and SVM-RFE algorithms, ID1, SCN4A, COL4A5, COLEC11, and SNAI2 were pinpointed as key genes associated with Atrial Fibrillation (AF). In both the training and validation datasets, these genes exhibited robust effectiveness. The immune infiltration analysis revealed that, in comparison to sinus rhythm (SR), atrial samples from patients with AF exhibited higher levels of neutrophils, while T cells follicular helper were relatively lower. Correlation analysis highlighted significant associations between ID1, SCN4A, COL4A5, COLEC11, SNAI2, and infiltrating immune cells. The outcomes of the RT- qPCR analysis in our investigation were consistent with the findings of bioinformatics analysis.
Conclusions: In summary, this study posits that ID1, SCN4A, COL4A5, COLEC11, and SNAI2 emerge as pivotal genes in Atrial Fibrillation (AF), exhibiting correlation with infiltrating immune cells. Furthermore, it underscores the indispensable roles played by infiltrating immune cells in the context of AF.