Language

English

Publication Date

7-1-2025

Journal

JACC: Basic to Translational Science

DOI

10.1016/j.jacbts.2025.02.004

PMID

40243956

PMCID

PMC12434206

PubMedCentral® Posted Date

4-16-2025

PubMedCentral® Full Text Version

Post-print

Abstract

Atrial fibrillation (AF) often coexists with heart failure, both involving inflammatory signaling and cardiac fibroblasts. To understand the role of fibroblast NLR family pyrin domain containing 3 (NLRP3) inflammasome in cardiac function, we found that NLRP3 was up-regulated in atrial fibroblasts from AF patients. Fibroblast-specific activation of NLRP3 in mice induced AF-promoting atrial myopathy and heart failure with diastolic dysfunction, accompanied by increased fibrosis, and reduced conduction velocity. Knockdown of NLRP3 prevented the AF-promoting atrial substrate and cardiomyopathy in the context of NLRP3 activation in fibroblasts. We identify the fibroblast NLRP3 inflammasome as a key pathway governing the promotion of proarrhythmic fibrosis in AF and cardiomyopathy.

Keywords

atrial cardiomyopathy, atrial fibrillation, cardiac fibroblast, fibrosis, inflammasome

Published Open-Access

yes

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