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


Journal

Biological & pharmaceutical bulletin
ISSN: 1347-5215
Titre abrégé: Biol Pharm Bull
Pays: Japan
ID NLM: 9311984

Informations de publication

Date de publication:
2019
Historique:
entrez: 2 4 2019
pubmed: 2 4 2019
medline: 2 8 2019
Statut: ppublish

Résumé

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

Identifiants

pubmed: 30930414
doi: 10.1248/bpb.b18-00363
doi:

Substances chimiques

CARD Signaling Adaptor Proteins 0
Ccl2 protein, mouse 0
Chemokine CCL2 0
Interleukin-1beta 0
NLR Family, Pyrin Domain-Containing 3 Protein 0
Nlrp3 protein, mouse 0
Pycard protein, mouse 0

Types de publication

Journal Article

Langues

eng

Pagination

543-546

Auteurs

Naoko Matsushita (N)

Division of Molecular and Cellular Pharmacology, Department of Pathophysiology and Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University.
Division of Cardiology, Department of Internal Medicine, School of Medicine, Iwate Medical University.

Nanae Ishida (N)

Division of Molecular and Cellular Pharmacology, Department of Pathophysiology and Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University.

Miho Ibi (M)

Division of Molecular and Cellular Pharmacology, Department of Pathophysiology and Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University.

Maki Saito (M)

Division of Molecular and Cellular Pharmacology, Department of Pathophysiology and Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University.

Masafumi Takahashi (M)

Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University.

Shunichiro Taniguchi (S)

Department of Molecular Oncology, Graduate School of Medicine, Shinshu University.

Yoichiro Iwakura (Y)

Division of Experimental Animal Immunology, Research Institute for Biological Sciences, Tokyo University of Science.

Yoshihiro Morino (Y)

Division of Cardiology, Department of Internal Medicine, School of Medicine, Iwate Medical University.

Eiichi Taira (E)

Department of Molecular Oncology, Graduate School of Medicine, Shinshu University.

Yohei Sawa (Y)

Division of Cardiology, Department of Internal Medicine, School of Medicine, Iwate Medical University.

Masamichi Hirose (M)

Division of Molecular and Cellular Pharmacology, Department of Pathophysiology and Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University.

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Classifications MeSH