Adiposity-associated atrial fibrillation: molecular determinants, mechanisms, and clinical significance

Research output: Contribution to journalReviewpeer-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 journalReviewpeer-review

Harvard

Gawalko, M, Saljic, A, Li, N, Abu-Taha, I, Jespersen, T, Linz, D, Nattel, S, Heijman, J, Fender, A & Dobrev, D 2023, 'Adiposity-associated atrial fibrillation: molecular determinants, mechanisms, and clinical significance', Cardiovascular Research, vol. 119, no. 3, pp. 614–630. https://doi.org/10.1093/cvr/cvac093

APA

Gawalko, M., Saljic, A., Li, N., Abu-Taha, I., Jespersen, T., Linz, D., Nattel, S., Heijman, J., Fender, A., & Dobrev, D. (2023). Adiposity-associated atrial fibrillation: molecular determinants, mechanisms, and clinical significance. Cardiovascular Research, 119(3), 614–630. https://doi.org/10.1093/cvr/cvac093

Vancouver

Gawalko M, Saljic A, Li N, Abu-Taha I, Jespersen T, Linz D et al. Adiposity-associated atrial fibrillation: molecular determinants, mechanisms, and clinical significance. Cardiovascular Research. 2023;119(3):614–630. https://doi.org/10.1093/cvr/cvac093

Author

Gawalko, Monika ; Saljic, Arnela ; Li, Na ; Abu-Taha, Issam ; Jespersen, Thomas ; Linz, Dominik ; Nattel, Stanley ; Heijman, Jordi ; Fender, Anke ; Dobrev, Dobromir. / Adiposity-associated atrial fibrillation : molecular determinants, mechanisms, and clinical significance. In: Cardiovascular Research. 2023 ; Vol. 119, No. 3. pp. 614–630.

Bibtex

@article{ae7cc39f9c14417e8c94b417f5288dc4,
title = "Adiposity-associated atrial fibrillation: molecular determinants, mechanisms, and clinical significance",
abstract = "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.",
keywords = "Adipokines, Atrial fibrillation, Epicardial adipose tissue, Obesity, NLRP3 inflammasome, Subcutaneous adipose tissue, Visceral adipose tissue, HIGH-FAT DIET, PERICARDIAL FAT, CARDIAC-HYPERTROPHY, TISSUE ACCUMULATION, BARIATRIC SURGERY, BODY-COMPOSITION, GENE-EXPRESSION, EPICARDIAL FAT, WEIGHT-LOSS, RISK-FACTOR",
author = "Monika Gawalko and Arnela Saljic and Na Li and Issam Abu-Taha and Thomas Jespersen and Dominik Linz and Stanley Nattel and Jordi Heijman and Anke Fender and Dobromir Dobrev",
year = "2023",
doi = "10.1093/cvr/cvac093",
language = "English",
volume = "119",
pages = "614–630",
journal = "Cardiovascular Research",
issn = "0008-6363",
publisher = "Oxford University Press",
number = "3",

}

RIS

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