Browning the Epicardial Adipose Tissues in Cardiovascular Regulation

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Browning the Epicardial Adipose Tissues in Cardiovascular Regulation

Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2019, Vol 12, Issue 4

Abstract

Epicardial adipose tissue (EAT) is located between the myocardium and the visceral layer of pericardium. EAT is characterized by increased rate of fatty acid metabolism and increased expression of thermogenic genes. EAT and the myocardium share the same microcirculation, suggesting a close interaction between them. Under normal physiological conditions, EAT produces anti-inflammatory or anti-atherosclerotic cytokines to exert its cardioprotective effects. Although many clinical studies have found significant associations between increased EAT mass and coronary artery disease (CAD). There is no direct evidence that inflammatory EAT worsens CAD. This short review focuses on the emerging physiological and pathophysiological role of EAT and potential pre-clinical application of EAT re-browning for treatment of cardiovascular disease.Epicardial adipose tissue (EAT) is the fat depot located between the myocardium and the visceral layer of the pericardium and generally exists in the atrioventricular and interventricular grooves [1,2]. The role of EAT within the heart is complicated, but can be commonly distinguished by mechanical, thermogenic, metabolic, and endocrine/paracrine functions [3,4]. EAT functions mechanically to protect the coronary artery against the torsion induced by the arterial pulse wave and myocardial contraction [5]. In addition, the studies from Sacks et al. had suggested that EAT functions similarly to brown adipose tissue (BAT) and yield heat directly to the myocardium conferring a survival benefit by protecting the heart from ischemia or hypoxia [6]. Higher expression levels of BAT-specific genes, such as uncoupling protein 1 (UCP1), PR domain containing 16 (PRDM16) and PPAR-γ coactivator-1α (PGC-1α) were observed in human EAT than in other fat depots [6]. Whether EAT is a BAT or functions as a BAT-like fat depot needs further investigation [7].Metabolically, EAT exhibits high rates of white adipose tissue (WAT) lipogenesis and lipolysis, acting as local triacylglycerol (TAG) store and as a buffer against toxic levels of FFA, in both myocardium and arteries [8]. EAT is abundant in saturated fatty acids and has the highest rate of free fatty acid (FFA) release and uptake of all fat depots [9,10]. It is widely known that the energy production in the heart is primarily generated by FFA oxidation, especially during the period of high demand [4,9]. EAT can produce several adipokines and inflammatory cytokines which generate potential interactions through apocrine or paracrine effect between EAT and myocardium [11,12]. Under normal physiological conditions, EAT produces anti-inflammatory or anti-atherosclerotic cytokines, such as adiponectin and adrenomedullin, to exert its cardioprotective effects [13,14]. Moreover, McAninch et al. had shown that EAT is a highly inflammatory tissue enriched with genes involved in coagulation, endothelial function, immune signaling and apoptosis compared to subcutaneous adipose tissue (SAT) [15].

Authors and Affiliations

Hui Chen Ku, Ching Feng Cheng

Keywords

Epicardial Adipose Tissue; Browning; Cardiovascular Disease; Ching Feng Cheng Myocardium Pericardium Thermogenic Contraction Hypoxia Lipogenesis Adrenomedullin Subcutaneous Cardiomyocyte

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EP ID EP587017
DOI 10.26717/BJSTR.2019.12.002271
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