The epicardial adipose tissue and the coronary arteries: dangerous liaisons
Author(s) -
Rosalinda Madonna,
Marika Massaro,
Egeria Scoditti,
Irene Pescetelli,
Raffaele De Caterina
Publication year - 2019
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvz062
Subject(s) - medicine , adipokine , coronary arteries , coronary artery disease , adipose tissue , paracrine signalling , proinflammatory cytokine , endocrine system , cardiology , artery , endocrinology , inflammation , insulin resistance , obesity , receptor , hormone
The adipose tissue (AT) is an endocrine organ that produces adipocytokines (adipokines), able to influence metabolic homeostasis. In the conventional classification, there are two large AT depots, characterized by different paracrine activities: the subcutaneous AT, which would mostly produce cytokines with protective properties against cardiovascular disease; and the visceral AT, responsible for the secretion of cytokines with proinflammatory, prothrombotic, and proatherogenic effects. A third component, the epicardial AT (EAT) is now receiving increasing attention due to its unique anatomical and functional proximity to the myocardium and the coronary arteries. In rodents, the EAT protects the heart from exposure to high levels of free fatty acids, and provides energy to the myocardium under high metabolic demands. The observation that atherosclerotic plaques are more prevalent in regions of coronary arteries surrounded by the EAT, while they tend to be less present in segments penetrating the myocardium (the septal branches and segments under myocardial bridges), has led to the hypothesis of a possible role of the EAT in promoting the development of atherosclerosis through endocrine and paracrine effects, in addition to the role of biomechanical forces affecting transendothelial lipid permeability into the intima. In this article, we review the clinical and molecular evidence linking the EAT and coronary artery disease through a systematic review of the literature. We, here, discuss current diagnostic techniques in evaluating the interaction between EAT and the onset of coronary artery disease and ischaemic heart disease. Finally, we review current knowledge on the underlying mechanisms by which the EAT may affect coronary atherosclerosis, and potential clinical implications of this interaction, making the EAT an attractive target for new therapeutics in cardiovascular disease.
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