Open AccessThe crosstalk between cardiomyocyte calcium and inflammasome signaling pathways in atrial fibrillation
Author(s) -
Xiaolei Wang,
Xiaohui Chen,
Dobromir Dobrev,
Na Li
Publication year - 2021
Publication title -
pflügers archiv für die gesamte physiologie des menschen und der tiere/pflügers archiv
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.428
H-Index - 129
eISSN - 0365-267X
pISSN - 0031-6768
DOI - 10.1007/s00424-021-02515-4
Subject(s) - crosstalk , inflammasome , atrial fibrillation , reentry , medicine , heart failure , pathogenesis , cardiology , neuroscience , receptor , psychology , physics , optics
Atrial fibrillation (AF) is the most frequent arrhythmia in adults. The prevalence and incidence of AF is going to increase substantially over the next few decades. Because AF increases the risk of stroke, heart failure, dementia, and others, it severely impacts the quality of life, morbidity, and mortality. Although the pathogenesis of AF is multifaceted and complex, focal ectopic activity and reentry are considered as the fundamental proarrhythmic mechanisms underlying AF development. Over the past 2 decades, large amount of evidence points to the key role of intracellular Ca 2+ dysregulation in both initiation and maintenance of AF. More recently, emerging evidence reveal that NLRP3 (NACHT, LRR, PYD domain-containing 3) inflammasome pathway contributes to the substrate of both triggered activity and reentry, ultimately promoting AF. In this article, we review the current state of knowledge on Ca 2+ signaling and NLRP3 inflammasome activity in AF. We also discuss the potential crosstalk between these two quintessential contributors to AF promotion.