Targeting the NLRP3 inflammasome signalling for the management of atrial fibrillation
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Targeting the NLRP3 inflammasome signalling for the management of atrial fibrillation. / Niskala, Alisha; Heijman, Jordi; Dobrev, Dobromir; Jespersen, Thomas; Saljic, Arnela.
In: British Journal of Pharmacology, 2024.Research output: Contribution to journal › Review › Research › peer-review
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TY - JOUR
T1 - Targeting the NLRP3 inflammasome signalling for the management of atrial fibrillation
AU - Niskala, Alisha
AU - Heijman, Jordi
AU - Dobrev, Dobromir
AU - Jespersen, Thomas
AU - Saljic, Arnela
N1 - Publisher Copyright: © 2024 The Author(s). British Journal of Pharmacology published by John Wiley & Sons Ltd on behalf of British Pharmacological Society.
PY - 2024
Y1 - 2024
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85196202691&partnerID=8YFLogxK
U2 - 10.1111/bph.16470
DO - 10.1111/bph.16470
M3 - Review
C2 - 38877789
AN - SCOPUS:85196202691
JO - British Journal of Pharmacology
JF - British Journal of Pharmacology
SN - 0007-1188
ER -
ID: 396860135