The epicardial adipose tissue and the coronary arteries: dangerous liaisons.


Journal

Cardiovascular research
ISSN: 1755-3245
Titre abrégé: Cardiovasc Res
Pays: England
ID NLM: 0077427

Informations de publication

Date de publication:
01 05 2019
Historique:
received: 11 12 2018
revised: 23 02 2019
accepted: 01 03 2019
pubmed: 25 3 2019
medline: 19 5 2020
entrez: 24 3 2019
Statut: ppublish

Résumé

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.

Identifiants

pubmed: 30903194
pii: 5418532
doi: 10.1093/cvr/cvz062
doi:

Substances chimiques

Adipokines 0
Inflammation Mediators 0

Types de publication

Journal Article Systematic Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

1013-1025

Informations de copyright

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com.

Auteurs

Rosalinda Madonna (R)

Center of Excellence on Aging (CeSI-Met), Institute of Cardiology, 'G. d'Annunzio' University, Via L. Polacchi, Chieti Scalo (Chieti), Italy.

Marika Massaro (M)

National Research Council (CNR), Department of Biomedical sciences, Institute of Clinical Physiology, Via Monteroni, Lecce, Italy.

Egeria Scoditti (E)

National Research Council (CNR), Department of Biomedical sciences, Institute of Clinical Physiology, Via Monteroni, Lecce, Italy.

Irene Pescetelli (I)

Center of Excellence on Aging (CeSI-Met), Institute of Cardiology, 'G. d'Annunzio' University, Via L. Polacchi, Chieti Scalo (Chieti), Italy.

Raffaele De Caterina (R)

Institute of Cardiology, University of Pisa, C/o Ospedale di Cisanello, Via Paradisa, 2, Pisa, Italy.

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