Unraveling the Role of Epicardial Adipose Tissue in Coronary Artery Disease: Partners in Crime?

• Published in: International journal of molecular sciences 2020-11, Vol.21 (22), p.8866
• Main Authors: Conceição, Glória, Martins, Diana, M Miranda, Isabel, Leite-Moreira, Adelino F, Vitorino, Rui, Falcão-Pires, Inês
• Format: Article
• Language: English
• Subjects: Adaptation; Adipocytes; Adipose tissue; Adipose Tissue - metabolism; Asymptomatic; Atherogenesis; Atherosclerosis; Bioinformatics; Body fat; Cardiovascular disease; Coronary artery; Coronary artery disease; Coronary Artery Disease - genetics; Coronary Artery Disease - metabolism; Coronary Artery Disease - pathology; Coronary vessels; Coronary Vessels - metabolism; Coronary Vessels - pathology; Crime; Diabetes; Genes; Heart; Heart diseases; Humans; Inflammation; Metabolism; Obesity; Pathophysiology; Pericardium - metabolism; Pericardium - pathology; Proteins; Proteome - genetics; Review; RNA, Messenger - genetics; Venn diagrams
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms21228866

The role of epicardial adipose tissue (EAT) in the pathophysiology of coronary artery disease (CAD) remains unclear. The present systematic review aimed at compiling dysregulated proteins/genes from different studies to dissect the potential role of EAT in CAD pathophysiology. Exhaustive literature research was performed using the keywords "epicardial adipose tissue and coronary artery disease", to highlight a group of proteins that were consistently regulated among all studies. Reactome, a pathway analysis database, was used to clarify the function of the selected proteins and their intertwined association. SignalP/SecretomeP was used to clarify the endocrine function of the selected proteins. Overall, 1886 proteins/genes were identified from 44 eligible studies. The proteins were separated according to the control used in each study (EAT non-CAD or subcutaneous adipose tissue (SAT) CAD) and by their regulation (up- or downregulated). Using a Venn diagram, we selected the proteins that were upregulated and downregulated (identified as 27 and 19, respectively) in EAT CAD for both comparisons. The analysis of these proteins revealed the main pathways altered in the EAT and how they could communicate with the heart, potentially contributing to CAD development. In summary, in this study, the identified dysregulated proteins highlight the importance of inflammatory processes to modulate the local environment and the progression of CAD, by cellular and metabolic adaptations of epicardial fat that facilitate the formation and progression of atherogenesis of coronaries.