{"@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/1360294646620046080.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1161/atvbaha.117.309451"}},{"identifier":{"@type":"URI","@value":"https://www.ahajournals.org/doi/full/10.1161/ATVBAHA.117.309451"}}],"dc:title":[{"@value":"Plasminogen Activator Inhibitor-1 Is a Marker and a Mediator of Senescence"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>PAI-1 (plasminogen activator inhibitor-1) is a member of the evolutionarily conserved serine protease inhibitor family and a potent and rapid-acting inhibitor of both of the mammalian plasminogen activators. Organismal homeostasis requires physiological levels of endogenous PAI-1, and increased PAI-1 production guides the onset and progression of numerous human diseases and contributes to the multimorbidity of aging. Both chronological and stress-induced accelerated aging are associated with cellular senescence and accompanied by marked increases in PAI-1 expression in tissues. Recent studies suggest that PAI-1 is not only a marker but also a key mediator of cellular senescence and organismal aging. Here, we review the significance of PAI-1 as a bonafide marker, as well as a critical mediator, of cellular senescence associated with aging and aging-related pathologies.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380294646620046083","@type":"Researcher","foaf:name":[{"@value":"Douglas E. Vaughan"}],"jpcoar:affiliationName":[{"@value":"From the Department of Medicine, Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, IL."}]},{"@id":"https://cir.nii.ac.jp/crid/1380294646620046080","@type":"Researcher","foaf:name":[{"@value":"Rahul Rai"}],"jpcoar:affiliationName":[{"@value":"From the Department of Medicine, Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, IL."}]},{"@id":"https://cir.nii.ac.jp/crid/1380294646620046084","@type":"Researcher","foaf:name":[{"@value":"Sadiya S. Khan"}],"jpcoar:affiliationName":[{"@value":"From the Department of Medicine, Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, IL."}]},{"@id":"https://cir.nii.ac.jp/crid/1380294646620046081","@type":"Researcher","foaf:name":[{"@value":"Mesut Eren"}],"jpcoar:affiliationName":[{"@value":"From the Department of Medicine, Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, IL."}]},{"@id":"https://cir.nii.ac.jp/crid/1380294646620046082","@type":"Researcher","foaf:name":[{"@value":"Asish K. Ghosh"}],"jpcoar:affiliationName":[{"@value":"From the Department of Medicine, Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, IL."}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"10795642"},{"@type":"EISSN","@value":"15244636"}],"prism:publicationName":[{"@value":"Arteriosclerosis, Thrombosis, and Vascular Biology"}],"dc:publisher":[{"@value":"Ovid Technologies (Wolters Kluwer Health)"}],"prism:publicationDate":"2017-08","prism:volume":"37","prism:number":"8","prism:startingPage":"1446","prism:endingPage":"1452"},"reviewed":"false","url":[{"@id":"https://www.ahajournals.org/doi/full/10.1161/ATVBAHA.117.309451"}],"createdAt":"2017-06-02","modifiedAt":"2024-05-12","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1050023186242771584","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Meta-analyses of epigenetic age acceleration and GrimAge components of schizophrenia or first-episode psychosis"}]},{"@id":"https://cir.nii.ac.jp/crid/1050583394472299648","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Biological aging analysis based on DNA methylation status for social anxiety disorder"}]},{"@id":"https://cir.nii.ac.jp/crid/1050856995321335296","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Epigenetic clock analysis and increased plasminogen activator inhibitor-1 in high-functioning autism spectrum disorder"}]},{"@id":"https://cir.nii.ac.jp/crid/1360298339699845632","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Expanded CUG Repeat RNA Induces Premature Senescence in Myotonic Dystrophy Model Cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1360584340517931392","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Accelerated epigenetic aging in alcohol dependence"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.1161/atvbaha.117.309451"},{"@type":"CROSSREF","@value":"10.3389/fgene.2022.865811_references_DOI_3ZjgEDtwExa0SPExkGQXWbxqKEA"},{"@type":"CROSSREF","@value":"10.1002/npr2.12487_references_DOI_3ZjgEDtwExa0SPExkGQXWbxqKEA"},{"@type":"CROSSREF","@value":"10.1371/journal.pone.0263478_references_DOI_3ZjgEDtwExa0SPExkGQXWbxqKEA"},{"@type":"CROSSREF","@value":"10.1016/j.jpsychires.2024.03.025_references_DOI_3ZjgEDtwExa0SPExkGQXWbxqKEA"},{"@type":"CROSSREF","@value":"10.1038/s41537-024-00531-8_references_DOI_3ZjgEDtwExa0SPExkGQXWbxqKEA"}]}