Figure 2.

Mechanisms and mediators of beneficial and deleterious effects of epicardial adipose tissue on cardiovascular risk. In healthy conditions, EAT shows protective functions by secreting cardioprotective adipokines, including anti-inflammatory and anti-atherogenic molecules (e.g., adiponectin and adrenomedullin), molecules related with glucose homeostasis (e.g., activin A and SFRP4), and molecules involved in vascular remodeling, blood pressure control, myocardial hypertrophy and adipogenesis (e.g., angiotensin, angiotensinogen, leptin). Under specific pathological conditions, including obesity, metabolic syndrome and type 2 diabetes, the beneficial properties of EAT might be impaired, and EAT might thus promote the development of cardiovascular disease, including CAD, HF, and AF, through multiple molecular mechanisms: reduced expression of adiponectin, increased expression of IL-6 and leptin, secretion of profibrotic factors, inflammatory markers, and FFAs, increase in catecholamine levels and in catecholamine biosynthetic enzymes, augmented ROS production, and fatty infiltration of the atrium. AF, atrial fibrillation; CAD, coronary artery disease; EAT, epicardial adipose tissue; FFAs, free fatty acids; HF, heart failure; ROS, reactive oxygen species; SFRP4, secreted frizzled-related protein 4; ↑ increased; ↓ decreased.