Role of PVAT in coronary atherosclerosis and vein graft patency: friend or foe?
Perivascular adipose tissue (PVAT) releases numerous factors and adipokines with paracrine effects on both vascular structure and function. These effects are variable as they depend on regional differences in PVAT among blood vessels and vary with changes in adiposity. There is considerable evidence demonstrating an association between coronary PVAT and the development and progression of coronary artery disease, which is associated with inflammation, oxidative stress, angiogenesis, vascular remodelling and blood clotting. However, PVAT also has a protective role in vascular grafts, especially the no-touch saphenous vein, in patients undergoing coronary artery bypass. This beneficial influence of PVAT involves factors such as adipocyte-derived relaxing factor, nitric oxide (NO), leptin, adiponectin, prostanoids, hydrogen sulphide and neurotransmitters, as well as mechanical protection. This article aims to highlight and compare the dual role of PVAT in the development and progression of coronary atherosclerosis, as well as in increased graft patency. Different deleterious and protective mechanisms of PVAT are also discussed and the inside-outside signalling paradigm of atherosclerosis development re-evaluated. The bidirectional communication between the arterial and venous wall and their surrounding PVAT, where signals originating from the vascular wall or lumen can affect PVAT phenotype, has been shown to be very complex. Moreover, signals from PVAT also influence the structure and function of the vascular wall in a paracrine manner.


BACKGROUND
This article is part of a themed section on Molecular Mechanisms Regulating Perivascular Adipose Tissue - Potential Pharmacological Targets? To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.20/issuetoc.
Instituto Pluridisciplinar and Facultad de Farmacia, Universidad Complutense, Madrid, Spain.
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MS
Fernández-Alfonso
Departamento de Ciencias Farmacéuticas y de la Salud, Facultad de Farmacia, Universidad CEU-San Pablo, Madrid, Spain.
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http://orcid.org/0000-0002-6366-8214
M
Gil-Ortega
Instituto Pluridisciplinar and Facultad de Farmacia, Universidad Complutense, Madrid, Spain.
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I
Aranguez
Department of Cardiothoracic and Vascular Surgery and University Health Care Research Center, School of Medical Sciences, Örebro University, Örebro, Sweden.
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D
Souza
Department of Cardiothoracic and Vascular Surgery and University Health Care Research Center, School of Medical Sciences, Örebro University, Örebro, Sweden.
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M
Dreifaldt
Departamento de Ciencias Farmacéuticas y de la Salud, Facultad de Farmacia, Universidad CEU-San Pablo, Madrid, Spain.
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Somoza
Royal Free Hospital Campus, University College Medical School, London, UK.
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MR
Dashwood
D000273:Adipose Tissue / Q000502:physiology*; D000818:Animals; D001158:Arteries / Q000502:physiology / Q000637:transplantation; D001026:Coronary Artery Bypass; D003324:Coronary Artery Disease / Q000503:physiopathology*; D006801:Humans; D014680:Veins / Q000502:physiology* / Q000637:transplantation