Publication Date
3-1-2021
Journal
Pflügers Archiv - European Journal of Physiology
DOI
10.1007/s00424-021-02515-4
PMID
33511453
PMCID
PMC7940593
PubMedCentral® Posted Date
3-1-2022
PubMedCentral® Full Text Version
Author MSS
Published Open-Access
yes
Keywords
Animals, Atrial Fibrillation, Calcium, Calcium Signaling, Humans, Inflammasomes, Myocytes, Cardiac, Signal Transduction, atrial fibrillation, calcium, NLRP3 inflammasome, delayed afterdepolarization, ryanodine receptor type-2, SERCA, sodium-calcium exchanger
Abstract
Atrial fibrillation (AF) is the most frequent arrhythmia in adults. The prevalence and incidence of AF is going to increase substantially over the next a 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 Ca2+ dysregulation in both initiation and maintenance of AF. More recently, emerging evidence reveal that NLRP3 (NACHT, LRR, PYD domain-containing 3) inflammasome pathways contribute to the substrate of both triggered activity and reentry, ultimately promoting AF. In this article, we review the current state of knowledge on Ca2+ signaling and NLRP3 inflammasome activity in AF. We also discuss the potential crosstalk between these two quintessential contributors to AF promotion.