{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1361981470262417536.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1073/pnas.1108586108"}},{"identifier":{"@type":"URI","@value":"https://pnas.org/doi/pdf/10.1073/pnas.1108586108"}}],"dc:title":[{"@value":"The inflammasome promotes adverse cardiac remodeling following acute myocardial infarction in the mouse"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>Acute myocardial infarction (AMI) initiates an intense inflammatory response that promotes cardiac dysfunction, cell death, and ventricular remodeling. The molecular events underlying this inflammatory response, however, are incompletely understood. In experimental models of sterile inflammation, ATP released from dying cells triggers, through activation of the purinergic P2X7 receptor, the formation of the inflammasome, a multiprotein complex necessary for caspase-1 activation and amplification of the inflammatory response. Here we describe the presence of the inflammasome in the heart in an experimental mouse model of AMI as evidenced by increased caspase-1 activity and cytoplasmic aggregates of the three components of the inflammasome—apoptosis speck-like protein containing a caspase-recruitment domain (ASC), cryopyrin, and caspase-1, localized to the granulation tissue and cardiomyocytes bordering the infarct. Cultured adult murine cardiomyocytes also showed the inducible formation of the inflammasome associated with increased cell death. P2X7 and cryopyrin inhibition (using silencing RNA or a pharmacologic inhibitor) prevented the formation of the inflammasome and limited infarct size and cardiac enlargement after AMI. The formation of the inflammasome in the mouse heart during AMI causes additional loss of functional myocardium, leading to heart failure. Modulation of the inflammasome may therefore represent a unique therapeutic strategy to limit cell death and prevent heart failure after AMI.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380013248227569031","@type":"Researcher","foaf:name":[{"@value":"Eleonora Mezzaroma"}],"jpcoar:affiliationName":[{"@value":"VCU Pauley Heart Center,"},{"@value":"VCU Victoria Johnson Center, and"},{"@value":"School of Pharmacy, Virginia Commonwealth University, Richmond, VA 23298"}]},{"@id":"https://cir.nii.ac.jp/crid/1380013248227569033","@type":"Researcher","foaf:name":[{"@value":"Stefano Toldo"}],"jpcoar:affiliationName":[{"@value":"VCU Pauley Heart Center,"},{"@value":"VCU Victoria Johnson Center, and"}]},{"@id":"https://cir.nii.ac.jp/crid/1380013248227569032","@type":"Researcher","foaf:name":[{"@value":"Daniela Farkas"}],"jpcoar:affiliationName":[{"@value":"VCU Victoria Johnson Center, and"}]},{"@id":"https://cir.nii.ac.jp/crid/1380013248227569030","@type":"Researcher","foaf:name":[{"@value":"Ignacio M. Seropian"}],"jpcoar:affiliationName":[{"@value":"VCU Pauley Heart Center,"},{"@value":"VCU Victoria Johnson Center, and"},{"@value":"School of Pharmacy, Virginia Commonwealth University, Richmond, VA 23298"}]},{"@id":"https://cir.nii.ac.jp/crid/1380013248227569028","@type":"Researcher","foaf:name":[{"@value":"Benjamin W. Van Tassell"}],"jpcoar:affiliationName":[{"@value":"VCU Victoria Johnson Center, and"},{"@value":"School of Pharmacy, Virginia Commonwealth University, Richmond, VA 23298"}]},{"@id":"https://cir.nii.ac.jp/crid/1380013248227569024","@type":"Researcher","foaf:name":[{"@value":"Fadi N. Salloum"}],"jpcoar:affiliationName":[{"@value":"VCU Pauley Heart Center,"}]},{"@id":"https://cir.nii.ac.jp/crid/1380013248227569026","@type":"Researcher","foaf:name":[{"@value":"Harsha R. Kannan"}],"jpcoar:affiliationName":[{"@value":"VCU Pauley Heart Center,"},{"@value":"VCU Victoria Johnson Center, and"}]},{"@id":"https://cir.nii.ac.jp/crid/1380013248227569029","@type":"Researcher","foaf:name":[{"@value":"Angela C. Menna"}],"jpcoar:affiliationName":[{"@value":"VCU Pauley Heart Center,"},{"@value":"VCU Victoria Johnson Center, and"}]},{"@id":"https://cir.nii.ac.jp/crid/1380013248227569025","@type":"Researcher","foaf:name":[{"@value":"Norbert F. Voelkel"}],"jpcoar:affiliationName":[{"@value":"VCU Pauley Heart Center,"},{"@value":"VCU Victoria Johnson Center, and"}]},{"@id":"https://cir.nii.ac.jp/crid/1380013248227569027","@type":"Researcher","foaf:name":[{"@value":"Antonio Abbate"}],"jpcoar:affiliationName":[{"@value":"VCU Pauley Heart Center,"},{"@value":"VCU Victoria Johnson Center, and"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00278424"},{"@type":"EISSN","@value":"10916490"},{"@type":"PISSN","@value":"https://id.crossref.org/issn/00278424"}],"prism:publicationName":[{"@value":"Proceedings of the National Academy of Sciences"}],"dc:publisher":[{"@value":"Proceedings of the National Academy of Sciences"}],"prism:publicationDate":"2011-11-21","prism:volume":"108","prism:number":"49","prism:startingPage":"19725","prism:endingPage":"19730"},"reviewed":"false","url":[{"@id":"https://pnas.org/doi/pdf/10.1073/pnas.1108586108"}],"createdAt":"2011-11-22","modifiedAt":"2024-04-14","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360005519846382976","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Cell-Specific Roles of NLRP3 Inflammasome in Myocardial Infarction"}]},{"@id":"https://cir.nii.ac.jp/crid/1360017280670447360","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"NLRP3 Inflammasome Activation Through Heart-Brain Interaction Initiates Cardiac Inflammation and Hypertrophy During Pressure Overload"}]},{"@id":"https://cir.nii.ac.jp/crid/1360285710936325120","@type":"Article","resourceType":"学術雑誌論文(journal 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