Inflammasome Signaling in Atrial Fibrillation: JACC State-of-the-Art Review

Amir Ajoolabady; Stanley Nattel; Gregory Y. H. Lip; Jun Ren

doi:10.1016/j.jacc.2022.03.379

Inflammasome Signaling in Atrial Fibrillation: JACC State-of-the-Art Review

Amir Ajoolabady, Stanley Nattel, Gregory Y. H. Lip^*, Jun Ren^*

^*Corresponding author for this work

Research output: Contribution to journal › Review article › peer-review

36 Citations (Scopus)

Abstract

As the most prevalent form of arrhythmia, atrial fibrillation (AF) increases the risk of heart failure, thromboembolism, and stroke, contributing to the raising mortality and morbidity in patients with cardiovascular diseases. Despite the multifaceted nature of AF pathogenesis and complexity of AF pathophysiology, a growing body of evidence indicates that the NLRP3 inflammasome activation contributes to onset and progression of AF. Herein, the authors aim at reviewing the current literature on the role of inflammasome signaling in AF pathogenesis, and novel therapeutic options in the management of AF.

Original language	English
Journal	Journal of the American College of Cardiology
Volume	79
Issue number	23
Pages (from-to)	2349-2366
Number of pages	18
ISSN	0735-1097
DOIs	https://doi.org/10.1016/j.jacc.2022.03.379
Publication status	Published - 14 Jun 2022

Bibliographical note

Keywords

Atrial Fibrillation/drug therapy
Heart Failure/etiology
Humans
Inflammasomes
Stroke/complications
Thromboembolism/etiology
atrial fibrillation
inflammation
NLRP3 inflammasome
interleukins

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Cite this

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title = "Inflammasome Signaling in Atrial Fibrillation: JACC State-of-the-Art Review",

abstract = "As the most prevalent form of arrhythmia, atrial fibrillation (AF) increases the risk of heart failure, thromboembolism, and stroke, contributing to the raising mortality and morbidity in patients with cardiovascular diseases. Despite the multifaceted nature of AF pathogenesis and complexity of AF pathophysiology, a growing body of evidence indicates that the NLRP3 inflammasome activation contributes to onset and progression of AF. Herein, the authors aim at reviewing the current literature on the role of inflammasome signaling in AF pathogenesis, and novel therapeutic options in the management of AF.",

keywords = "Atrial Fibrillation/drug therapy, Heart Failure/etiology, Humans, Inflammasomes, Stroke/complications, Thromboembolism/etiology, atrial fibrillation, inflammation, NLRP3 inflammasome, interleukins",

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AU - Ren, Jun

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AB - As the most prevalent form of arrhythmia, atrial fibrillation (AF) increases the risk of heart failure, thromboembolism, and stroke, contributing to the raising mortality and morbidity in patients with cardiovascular diseases. Despite the multifaceted nature of AF pathogenesis and complexity of AF pathophysiology, a growing body of evidence indicates that the NLRP3 inflammasome activation contributes to onset and progression of AF. Herein, the authors aim at reviewing the current literature on the role of inflammasome signaling in AF pathogenesis, and novel therapeutic options in the management of AF.

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KW - Heart Failure/etiology

KW - Humans

KW - Inflammasomes

KW - Stroke/complications

KW - Thromboembolism/etiology

KW - atrial fibrillation

KW - inflammation

KW - NLRP3 inflammasome

KW - interleukins

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