Exploring the Role of Epicardial Adipose Tissue in Coronary Artery Disease From the Difference of Gene Expression

Objectives Epicardial adipose tissue (EAT) is closely adjacent to the coronary arteries and myocardium, its role as an endocrine organ to affect the pathophysiological processes of the coronary arteries and myocardium has been increasingly recognized. However, the specific gene expression profiles of EAT in coronary artery disease (CAD) has not been well characterized. Our aim was to investigate the role of EAT in CAD at the gene level. Methods Here, we compared the histological and gene expression difference of EAT between CAD and non-CAD. We investigated the gene expression profiles in the EAT of patients with CAD through the high-throughput RNA sequencing. We performed bioinformatics analysis such as functional enrichment analysis and protein-protein interaction network construction to obtain and verify the hub differentially expressed genes (DEGs) in the EAT of CAD. Results Our results showed that the size of epicardial adipocytes in the CAD group was larger than in the control group. Our findings on the EAT gene expression profiles of CAD showed a total of 747 DEGs (fold change >2, p value <0.05). The enrichment analysis of DEGs showed that more pro-inflammatory and immunological genes and pathways were involved in CAD. Ten hub DEGs (GNG3, MCHR1, BDKRB1, MCHR2, CXCL8, CXCR5, CCR8, CCL4L1, TAS2R10, and TAS2R41) were identified. Conclusion Epicardial adipose tissue in CAD shows unique gene expression profiles and may act as key regulators in the CAD pathological process.

Automated summary

This study compared the histological and gene expression differences of epicardial adipose tissue (EAT) between patients with and without coronary artery disease (CAD). The CAD group showed larger epicardial adipocytes and a total of 747 differentially expressed genes (DEGs) were identified in CAD EAT, with more pro-inflammatory and immunological genes and pathways involved. Ten hub DEGs were also identified. EAT in CAD exhibits unique gene expression profiles and may play a key role in the pathological process of CAD.