# Omics Insights into Epicardial Adipose Tissue: Unravelling Its Molecular Landscape
## 3 Genomics and Transcriptomics of EAT
Perivascular EAT overexpressed genes responsible for regulating vascular morphology, angiogenesis, inflammation and haemostasis, emphasizing the role of cross talk between EAT and vessel wall in atherosclerosis [67]. However, transferring this knowledge into clinical practice is hard, since serum inflammatory markers are not specific for a certain local inflammation site [18], making it challenging to find a marker for inflammation that reports changes in EAT metabolism. Moreover, hsCRP, homocysteine, insufficient vitamin D levels and TNF-\(\alpha\) have similar circulating levels in patients with CAD versus the control group [68]. One study suggests the possibility of clinically assessing EAT dysfunctionality by measuring circulating CCL13, which is the only chemokine that presents a significant increase both in plasma and in EAT in patients with CAD, presenting a sensitivity of 73% and a specificity of 67% as a biomarker. miR-103-3p has been found to be a modulator of CCL13 in CAD [39]. Other findings emphasize na MCP-1 expression significantly up-regulated in CAD patients after adjusting for cofounders like hypertension, diabetes, dyslipidemia, age, gender, and BMI, together with the down-regulation of adiponectin as a protective molecule [68]. To further emphasize the inflammatory pathway in CAD, EAT describes an increased expression of sPLA\({}_{2}\)-IIA (secretory type II phospholipase A\({}_{2}\)), which is responsible for catalysing the rate-limiting step in the synthesis of proinflammatory lipid mediators [66]. \begin{table}
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We should be careful in interpreting these results, since inflammation seems to be associated with a proper adipose tissue function, and therefore the presence of inflammatory infiltrates does not necessarily assess the presence of the disease [69]. Nevertheless, the inflammatory profile of EAT seems to be altered in the presence of obesity or diabetes, rather than in the presence of cardiac disease [5]. At the same time, atherosclerotic plaque develops only in sections of coronary arteries that are surrounded completely by EAT to an extent that the amount of fat correlates with the width and composition of the plaque [70; 71]. Therefore, it is still challenging to determine the precise factors that trigger EAT changes and whether they represent a cause or a consequence of diseases. Considering the proximity of EAT and the myocardium, the exosomal miRNAs secreted by adipose tissue could be taken up by myocytes. Few studies have been performed on the role of EVs in CVD. The first study of this kind addressing the pathogenesis of atrial fibrillation was conducted in 2021 and described a proinflammatory, profibrotic and proarrhythmic profile of EVs from EAT in patients with fibrillation [72]. [PERSON] et al. analysed the secretome of EAT and showed that EVs which are more concentrated in the EAT than in the SAT secretome are involved in the physiopathology of atrial fibrillation by shortening the repolarization action's potential duration to 80%. EAT secretome overexresses miR-1-3p and miR-133a-3p, which down-regulates Kcnj2 gene expression related to cardiac electrophysiology, therefore leading to a reduced arrhythmogenic conduction and suggesting new therapeutic targets for fibrillation [37; 73; 74]. Moreover, the distinct pre-operatory transcriptome of EAT described a pre-existing inflammatory state in subjects that developed postoperative atrial fibrillation (POAF) [75]. POAF emerges as the predominant complication and a significant predictor of mortality and morbidity in the immediate period following cardiac surgery [76]. A recent study profiled for the first time the expression of lncRNA in EAT of patients with atrial fibrillation.