Adiposity-associated atrial fibrillation: molecular determinants, mechanisms, and clinical significance
Research output: Contribution to journal › Review › peer-review
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Adiposity-associated atrial fibrillation : molecular determinants, mechanisms, and clinical significance. / Gawalko, Monika; Saljic, Arnela; Li, Na; Abu-Taha, Issam; Jespersen, Thomas; Linz, Dominik; Nattel, Stanley; Heijman, Jordi; Fender, Anke; Dobrev, Dobromir.
In: Cardiovascular Research, Vol. 119, No. 3, 2023, p. 614–630.Research output: Contribution to journal › Review › peer-review
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TY - JOUR
T1 - Adiposity-associated atrial fibrillation
T2 - molecular determinants, mechanisms, and clinical significance
AU - Gawalko, Monika
AU - Saljic, Arnela
AU - Li, Na
AU - Abu-Taha, Issam
AU - Jespersen, Thomas
AU - Linz, Dominik
AU - Nattel, Stanley
AU - Heijman, Jordi
AU - Fender, Anke
AU - Dobrev, Dobromir
PY - 2023
Y1 - 2023
N2 - Obesity is an important contributing factor to the pathophysiology of atrial fibrillation (AF) and its complications by causing systemic changes, such as altered haemodynamic, increased sympathetic tone, and low-grade chronic inflammatory state. In addition, adipose tissue is a metabolically active organ that comprises various types of fat deposits with discrete composition and localization that show distinct functions. Fatty tissue differentially affects the evolution of AF, with highly secretory active visceral fat surrounding the heart generally having a more potent influence than the rather inert subcutaneous fat. A variety of proinflammatory, profibrotic, and vasoconstrictive mediators are secreted by adipose tissue, particularly originating from cardiac fat, that promote atrial remodelling and increase the susceptibility to AF. In this review, we address the role of obesity-related factors and in particular specific adipose tissue depots in driving AF risk. We discuss the distinct effects of key secreted adipokines from different adipose tissue depots and their participation in cardiac remodelling. The possible mechanistic basis and molecular determinants of adiposity-related AF are discussed, and finally, we highlight important gaps in current knowledge, areas requiring future investigation, and implications for clinical management.
AB - Obesity is an important contributing factor to the pathophysiology of atrial fibrillation (AF) and its complications by causing systemic changes, such as altered haemodynamic, increased sympathetic tone, and low-grade chronic inflammatory state. In addition, adipose tissue is a metabolically active organ that comprises various types of fat deposits with discrete composition and localization that show distinct functions. Fatty tissue differentially affects the evolution of AF, with highly secretory active visceral fat surrounding the heart generally having a more potent influence than the rather inert subcutaneous fat. A variety of proinflammatory, profibrotic, and vasoconstrictive mediators are secreted by adipose tissue, particularly originating from cardiac fat, that promote atrial remodelling and increase the susceptibility to AF. In this review, we address the role of obesity-related factors and in particular specific adipose tissue depots in driving AF risk. We discuss the distinct effects of key secreted adipokines from different adipose tissue depots and their participation in cardiac remodelling. The possible mechanistic basis and molecular determinants of adiposity-related AF are discussed, and finally, we highlight important gaps in current knowledge, areas requiring future investigation, and implications for clinical management.
KW - Adipokines
KW - Atrial fibrillation
KW - Epicardial adipose tissue
KW - Obesity
KW - NLRP3 inflammasome
KW - Subcutaneous adipose tissue
KW - Visceral adipose tissue
KW - HIGH-FAT DIET
KW - PERICARDIAL FAT
KW - CARDIAC-HYPERTROPHY
KW - TISSUE ACCUMULATION
KW - BARIATRIC SURGERY
KW - BODY-COMPOSITION
KW - GENE-EXPRESSION
KW - EPICARDIAL FAT
KW - WEIGHT-LOSS
KW - RISK-FACTOR
U2 - 10.1093/cvr/cvac093
DO - 10.1093/cvr/cvac093
M3 - Review
C2 - 35689487
VL - 119
SP - 614
EP - 630
JO - Cardiovascular Research
JF - Cardiovascular Research
SN - 0008-6363
IS - 3
ER -
ID: 317371761