| Summary: | Obesity is an independent risk factor for atrial fibrillation (AF). However, the mechanisms underlying this crosstalk are still being uncovered. Co-differentially expressed genes (co-DEGs) of AF and obesity microarrays were identified by bioinformatics analysis. Subsequently, functional enrichment, cell-type enrichment, and protein–protein interaction network analyses of co-DEGs were carried out. Then, we validated the hub genes by qRT-PCR of patients’ blood samples. Finally, CIBERSORT was utilized to evaluate the AF microarray to determine immune infiltration and the correlation between validated hub genes and immune cells. A total of 23 co-up-regulated DEGs in AF and obesity microarrays were identified, and these genes were enriched in inflammation- and immune-related function. The enriched cells were whole blood, CD33+ myeloid, and CD14+ monocytes. The hub genes were identified as <i>MNDA</i>, <i>CYBB</i>, <i>CD86</i>, <i>FCGR2C</i>, <i>NCF2</i>, <i>LCP2</i>, <i>TLR8</i>, <i>HLA-DRA</i>, <i>LCP1</i>, and <i>PTPN22</i>. All hub genes were only elevated in blood samples of obese-AF patients. The CIBERSORT analysis revealed that the AF patients’ left atrial appendage had increased infiltration of naïve B cells and decreased infiltration of memory B cells. The hub genes were related positively to naïve B cells and negatively to memory B cells. Ten hub genes may serve as biomarkers for obesity-related AF. These findings may also aid in comprehending pathophysiological mechanisms for obesity-related AF.
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