IL-1β Plays an Important Role in Pressure Overload-Induced Atrial Fibrillation in Mice

IL-1β Plays an Important Role in Pressure Overload-Induced Atrial Fibrillation in Mice
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DOI:
10.1248/bpb.b18-00363
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发表时间:
2019-04-01
影响因子:
2
通讯作者:
Hirose, Masamichi
Hirose, Masamichi
中科院分区:
医学4区
文献类型:
--
作者:
Matsushita, Naoko;Ishida, Nanae;Hirose, Masamichi

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Hypertension is one risk for atrial fibrillation (AF) and induces cardiac inflammation. Recent evidence indicates that pressure overload-induced ventricular structural remodeling is associated with the activation of nucleotide binding-oligomerization domain (NOD)-like receptor P3 (NLRP3) inflammasomes, including an apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC). We hypothesized that NLRP3 inflammasomes are an initial sensor for danger signals in pressure overload-induced atrial remodeling, leading to AF. Transverse aortic constriction (TAC) or a sham procedure was performed in mice deficient for ASC(-/-) and interleukin-1 beta (IL-1 beta(-/-)). One week after the procedure, electrical left atrial burst pacing from the esophagus was performed for 30s to induce AF. IL-1 beta, monocyte chemotactic protein 1 (MCP-1), connective tissue growth factor (CTGF), and collagen 1 gene expression were also examined. The electrical burst pacing induced AF in TAC-operated wild-type (WT) (p