# Omics Insights into Epicardial Adipose Tissue: Unravelling Its Molecular Landscape
## 3 Genomics and Transcriptomics of EAT
In patients undergoing coronary artery bypass grafting surgery, the ADORA1 (adenosine A1 receptor) gene involved in myocardial ischemia and PTGDS (prostaglandin D2 synthase) gene associated with the progression of atherosclerosis have a significantly up-regulated expression in EAT versus SAT [57]. One study identified 14 genes (4 up-regulated, 10 down-regulated), which can discriminate EAT from SAT with 100% accuracy, independently of the patients' disease [39]. The data emphasize in the end the irreplaceable role of EAT, and its special characteristics as a tissue with a more pronounced inflammatory profile than SAT even in the absence of CAD. One study reports that inflammation is the result of differences in gene expression dictated by EAT itself and not by the disease [58]. A comprehensive bioinformatic analysis merged the expression profiles from these three studies [39; 57; 58] and identified differentially expressed genes between EAT and SAT, with 10 hub genes being involved in CAD development: HOXA5, HOXB5, HOXC6, HOXC8, HOXB7, COL1A1, CCND1, CCL2, HP and TWIST1. The study confirms the upregulation of pro-inflammatory and immunological pathways in the process of CAD, while the intestinal immune system, coagulation cascade, complement function and vascular endothelial growth factor production seem to also have a role in EAT metabolism. To enhance precision, these results were further validated in the same study on samples from eight patients with CAD [59]. \begin{table}
\begin{tabular}{c c c c} \hline \hline \multirow{2}{*}{**Gene/Product Name**} & **mRNA Expression in** & & \\  & **Diabetic EAT vs.** & & **Biological Process** & **Reference** \\  & **Non-Diabetic EAT** & & & \\ \hline PTX9 (pentraxin-related protein 3) & Up-regulated in diabetic EAT vs. diabetic SAT & complement component C1q complex & \\  & & binding, beta-D-glucan binding & \\ \hline LIPG (endothelial lipase G) & Up-regulated in diabetic EAT vs. diabetic SAT & phospholipase and triglyceride lipase & \\  & & activity, heparin binding, lipid metabolic & \\  & & process, response to nutrient & \\ \hline UCP-1 (mitochondrial brown fat & Down-regulated in diabetic & oxidative phosphorylation uncoupler & \\  & with CAD EAT vs. non-diabetic & activity, GTP binding, long-chain & \\  & & with CAD EAT & fatty-acid binding, cardiolip binding, & \\  & & diet-induced thermogenesis & \\ \hline PGC1\(\alpha\) (peroxisome & Down-regulated in diabetic & negative regulation of smooth muscle & \\  & with CAD EAT vs. non-diabetic & cell proliferation, energy homeostasis, & \\  & & with CAD EAT & transcription coactivator activity & \\ \hline \hline \end{tabular}
\end{table} 
Table 1: _Cont._
\begin{table}
\begin{tabular}{c c c c c c c} \hline \hline
**Gene/Product Name** & **mRNA Expression in CAD EAT vs. Control** & **mRNA Expression in CAD EAT vs. CAD SAT** & **EAT Anatomical Location** & **Reference** & **Conclusion** \\ \hline \multirow{3}{*}{Chemerin} & \multirow{3}{*}{Up-regulated} & \multirow{3}{*}{Up-regulated} & \multirow{3}{*}{Up-regulated} & Near the proximal right coronary artery & [PERSON] et al. (2020) & the severity of CAD is positively associated with the level of chemerin mRNA in EAT and not with its circulating level \\ \hline \multirow{3}{*}{Adiponectin} & \multirow{3}{*}{Down-regulated} & \multirow{3}{*}{Down-regulated} & Near the left anterior descending artery & \multirow{3}{*}{[PERSON] et al. (2021)} & adiponectin might inhibit atherosclerosis through decreasing TLR expression on macrophage/monocytes \\ \cline{3-5}  & & & & & \\ \cline{3-5}  & & & & & \\ \cline{3-5}  & & & & & \\ \cline{3-5}  & & & & & & \\ \cline{3-5}  & & & & & & \\ \cline{3-5}  & & & & & & \\ \hline \multirow{3}{*}{Adiponectin} & \multirow{3}{*}{Down-regulated} & \multirow{3}{*}{Down-regulated} & \multirow{3}{*}{Down-regulated} & Near the right coronary artery & \multirow{3}{*}{[PERSON] et al. (2021)} & \multirow{3}{*}{[PERSON].