Inflammation, a link between obesity and atrial fibrillation

Despite the long belief that the role of the adipose tissue was restricted to that of a passive store of triglycerides and a rich source of fatty acids, accumulating data demonstrates that the adipose tissue acts as an endocrine organ, capable of producing a large number of cytokines incriminated in...

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Bibliographic Details
Published in:Inflammation research 2015-06, Vol.64 (6), p.383-393
Main Authors: Scridon, Alina, Dobreanu, Dan, Chevalier, Philippe, Şerban, Răzvan Constantin
Format: Article
Language:English
Subjects:
Adipokines - metabolism
Adipokines - physiology
Allergology
Animals
Atrial Fibrillation - etiology
Atrial Fibrillation - physiopathology
Biomedical and Life Sciences
Biomedicine
Dermatology
Humans
Immunology
Inflammation - complications
Inflammation - physiopathology
Neurology
Obesity - etiology
Obesity - physiopathology
Pharmacology/Toxicology
Review
Rheumatology
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Summary:Despite the long belief that the role of the adipose tissue was restricted to that of a passive store of triglycerides and a rich source of fatty acids, accumulating data demonstrates that the adipose tissue acts as an endocrine organ, capable of producing a large number of cytokines incriminated in generating a systemic inflammatory status. At its turn, this adiposity-related pro-inflammatory status appears to promote a large range of cardiovascular disorders, including atrial fibrillation (AF). Recent studies suggest that, in addition to systemic adiposity, the volume of the pericardial fat of the entire heart, and particularly of that overlying the atria, may represent an even more important risk factor for AF. This review focuses on the most relevant clinical and experimental data that bridge adiposity-induced inflammation and AF, and provides, through a multidisciplinary approach, a discussion that integrates both the current knowledge regarding the prolific activity of systemic and pericardial adipose tissue as sources of inflammatory mediators and the main effects of adiposity-induced inflammation on the most relevant electrophysiological, structural, and autonomic mechanisms responsible for AF.
ISSN:1023-3830
1420-908X
DOI:10.1007/s00011-015-0827-8