Epicardial adipose tissue has a unique transcriptome modified in severe coronary artery disease

Abstract

ObjectiveTo explore the transcriptome of epicardial adipose tissue (EAT) as compared to subcutaneous adipose tissue (SAT) and its modifications in a small number of patients with coronary artery disease (CAD) versus valvulopathy.Design and MethodsSAT and EAT samples were obtained during elective cardiothoracic surgeries. The transcriptome of EAT was evaluated using an unbiased, whole-genome approach as compared to SAT in subjects with CAD (n=6) and without CAD (n=5), where the patients without CAD had cardiac valvulopathy.ResultsRelative to SAT, EAT is a highly inflammatory tissue enriched with genes involved in endothelial function, coagulation, immune signaling, potassium transport and apoptosis. EAT is lacking in expression of genes involved in protein metabolism, TGF-beta signaling, and oxidative stress. Although underpowered, in subjects with severe CAD, there is an expression trend suggesting widespread downregulation of EAT encompassing a diverse group of gene sets related to intracellular trafficking, proliferation/transcription regulation, protein catabolism, innate immunity/lectin pathway and ER stress.ConclusionsThe EAT transcriptome is unique when compared to SAT. In the setting of CAD versus valvulopathy, there is possible alteration of the EAT transcriptome with gene suppression. This pilot study explores the transcriptome of EAT in CAD and valvulopathy, providing new insight into its physiologic and pathophysiologic roles.

‘Browning’ the cardiac and peri-vascular adipose tissues to modulate cardiovascular risk

“…In support of this theory is evidence that the EAT of individuals with CAD is associated with a brown-to-white trans-differentiation characterised by significant decreases in thermogenic genes and upregulation of white adipogenesis [66]. This brown-to-white phenotype is associated with a significant increase in EAT reactive oxygen species production [66] whilst the EAT transcriptome is also characterised by markers of inflammation [67]. Furthermore, the association between EAT expression of UCP1 and circulating HDL/triglycerides suggests that functional brown adipocytes in this depot could modulate lipid metabolism in humans [37].…”

Hyperglycemia-induced changes in miRNA expression patterns in epicardial adipose tissue of piglets

“…There are few microarray studies of EAT's transcriptome in human and other large mammals, especially pig. McAninch and coworkers indicate the genome-wide mRNA profile of EAT versus SAT in patients with coronary artery disease (CAD) and found enrichment in genes involved in endothelial function, coagulation, or immune signaling, and lack of expression of genes associated with protein metabolism and oxidative stress (McAninch et al 2015). It has been investigated that similar interactions might exist in the adipose tissue depots in a pig model of familial hypercholesterolemia with CAD (Company et al 2010).…”

Epicardial Fat Thickness in Patients with Autosomal Dominant Polycystic Kidney Disease

“…Remarkably, EAT is a highly inflammatory fat depot that plays a key pathogenic role in conditions that are not necessarily linked to obesity, such as coronary artery disease and CKD [28]. EAT has a unique proteasome and transcriptome highly enriched in genes encoding for inflammatory factors, as recently described by Iacobellis and colleagues [29]. Ultrasound-measured EAT thickness showed a correlation with circulating inflammatory markers [13, 14, 18].…”