Abstract
The epicardial adipose tissue (EAT) is the visceral fat depot of the heart which is highly plastic and in direct contact with myocardium and coronary arteries. Because of its singular proximity with the myocardium, the adipokines and pro-inflammatory molecules secreted by this tissue may directly affect the metabolism of the heart and coronary arteries. Its accumulation, measured by recent new non-invasive imaging modalities, has been prospectively associated with the onset and progression of coronary artery disease (CAD) and atrial fibrillation in humans. Recent studies have shown that EAT exhibits beige fat-like features, and express uncoupling protein 1 (UCP-1) at both mRNA and protein levels. However, this thermogenic potential could be lost with age, obesity and CAD. Here we provide an overview of the physiological and pathophysiological relevance of EAT and further discuss whether its thermogenic properties may serve as a target for obesity therapeutic management with a specific focus on the role of immune cells in this beiging phenomenon.
Highlights
IntroductionPublisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations
In a study using cold-pressor test, we previously showed, in healthy lean volunteers, a negative correlation between epicardial adipose tissue (EAT) amount and microvascular coronary vasodilation, an abnormality that can be detectable before the apparition of coronary artery disease (CAD), suggesting that EAT could be involved in endothelial dysfunction [70]
They demonstrated that the brown adipose tissues (BAT)-specific genes uncoupling protein 1 (UCP-1), PGC-1α, PRDM16 and bone morphogenetic protein 7 (BMP7) were statistically significant lower in CAD patients and white adipose tissue (WAT)-specific gene insulin-like growth factor binding protein 3 (IGFBP3) and HOXC9 were significantly higher compared to non-CAD patients, which suggests a change in the composition of the EAT in CAD patients
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. EAT is characterized by its cardioprotective functions in physiological conditions and its increased expression of thermogenic genes giving its adipocytes a beige/brite phenotype. This metabolically active tissue has endocrine properties, and a special location that makes it able to modulate the structure and function of the myocardium. Transcriptional studies revealed that EAT exhibits high expression of the beige adipocyte-specific marker CD137, and thermogenic genes such as UCP-1, PRDM16, PGC-1α, PPARγ and BAT-specific genes such as actin alpha 1 (ACTA1), PPARγ co-activator 1 alpha (PPARGC1A), troponin. We will focus on the beiging or browning of EAT in cardiovascular and metabolic diseases and its link with immune cells
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