Targeting the NLRP3 inflammasome signalling for the management of atrial fibrillation

Inflammatory signalling via the nod‐like receptor (NLR) family pyrin domain‐containing protein‐3 (NLRP3) inflammasome has recently been implicated in the pathophysiology of atrial fibrillation (AF). However, the precise role of the NLRP3 inflammasome in various cardiac cell types is poorly understoo...

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Bibliographic Details
Published in:British journal of pharmacology 2024-12, Vol.181 (24), p.4939-4957
Main Authors: Niskala, Alisha, Heijman, Jordi, Dobrev, Dobromir, Jespersen, Thomas, Saljic, Arnela
Format: Article
Language:English
Subjects:
Animals
Atrial Fibrillation - drug therapy
Atrial Fibrillation - immunology
Atrial Fibrillation - metabolism
Cardiomyocytes
Colchicine
Drug development
Fibrillation
Humans
Inflammasomes
Inflammasomes - antagonists & inhibitors
Inflammasomes - metabolism
Inflammation
Leukocytes (neutrophilic)
Macrophages
Monocytes
NLR Family, Pyrin Domain-Containing 3 Protein - antagonists & inhibitors
NLR Family, Pyrin Domain-Containing 3 Protein - metabolism
Pyrin protein
Reviews
Signal transduction
Signal Transduction - drug effects
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Summary:Inflammatory signalling via the nod‐like receptor (NLR) family pyrin domain‐containing protein‐3 (NLRP3) inflammasome has recently been implicated in the pathophysiology of atrial fibrillation (AF). However, the precise role of the NLRP3 inflammasome in various cardiac cell types is poorly understood. Targeting components or products of the inflammasome and preventing their proinflammatory consequences may constitute novel therapeutic treatment strategies for AF. In this review, we summarise the current understanding of the role of the inflammasome in AF pathogenesis. We first review the NLRP3 inflammasome pathway and inflammatory signalling in cardiomyocytes, (myo)fibroblasts and immune cells, such as neutrophils, macrophages and monocytes. Because numerous compounds targeting NLRP3 signalling are currently in preclinical development, or undergoing clinical evaluation for other indications than AF, we subsequently review known therapeutics, such as colchicine and canakinumab, targeting the NLRP3 inflammasome and evaluate their potential for treating AF.
ISSN:0007-1188
1476-5381
1476-5381
DOI:10.1111/bph.16470