{"@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/1362825895623777280.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1161/strokeaha.108.531632"}},{"identifier":{"@type":"URI","@value":"https://www.ahajournals.org/doi/full/10.1161/STROKEAHA.108.531632"}}],"dc:title":[{"@value":"Apoptotic Mechanisms After Cerebral Ischemia"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>\n            <jats:bold>\n              <jats:italic>Background and Purpose—</jats:italic>\n            </jats:bold>\n            Traditionally, cell death after cerebral ischemia was considered to be exclusively necrotic in nature, but research over the past decade has revealed that after a stroke, many neurons in the ischemic penumbra will undergo apoptosis.\n          </jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Summary of Review—</jats:italic>\n            </jats:bold>\n            This brief review provides a general overview and update of various signaling pathways in the development of apoptosis in ischemic lesions. Cerebral ischemia triggers two general pathways of apoptosis: the intrinsic pathway, originating from mitochondrial release of cytochrome\n            <jats:italic>c</jats:italic>\n            and associated stimulation of caspase-3; and the extrinsic pathway, originating from the activation of cell surface death receptors, resulting in the stimulation of caspase-8. Although many of the key apoptotic proteins have been identified, our understanding of the complex underlying mechanisms remains poor and hence treatment of stroke patients by manipulating apoptotic pathways remains a daunting task. However, recent advances in the field have helped broaden our knowledge of apoptosis after cerebral ischemia. Further to the simplistic concept that stroke-induced apoptosis occurs predominantly in neurons and is caspase-dependent, accumulating evidence now indicates that apoptosis is prevalent in nonneuronal cells and that caspase-independent mechanisms also play a key role.\n          </jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Conclusions—</jats:italic>\n            </jats:bold>\n            Although the ischemic penumbra is under threat of infarction, it is potentially salvageable and thus represents an opportunity for therapeutic intervention.\n          </jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1382825895623777280","@type":"Researcher","foaf:name":[{"@value":"Brad R.S. Broughton"}],"jpcoar:affiliationName":[{"@value":"From the Department of Pharmacology (B.R.S.B., C.G.S.), Monash University, Victoria, Australia; and the Southern Clinical School (D.C.R.), Monash University, Clayton, Australia."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895623777282","@type":"Researcher","foaf:name":[{"@value":"David C. Reutens"}],"jpcoar:affiliationName":[{"@value":"From the Department of Pharmacology (B.R.S.B., C.G.S.), Monash University, Victoria, Australia; and the Southern Clinical School (D.C.R.), Monash University, Clayton, Australia."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895623777281","@type":"Researcher","foaf:name":[{"@value":"Christopher G. Sobey"}],"jpcoar:affiliationName":[{"@value":"From the Department of Pharmacology (B.R.S.B., C.G.S.), Monash University, Victoria, Australia; and the Southern Clinical School (D.C.R.), Monash University, Clayton, Australia."}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00392499"},{"@type":"EISSN","@value":"15244628"}],"prism:publicationName":[{"@value":"Stroke"}],"dc:publisher":[{"@value":"Ovid Technologies (Wolters Kluwer Health)"}],"prism:publicationDate":"2009-05","prism:volume":"40","prism:number":"5","prism:startingPage":"e331"},"reviewed":"false","url":[{"@id":"https://www.ahajournals.org/doi/full/10.1161/STROKEAHA.108.531632"}],"createdAt":"2009-01-30","modifiedAt":"2024-05-13","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360004232392003840","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Heptamethoxyflavone, a citrus flavonoid, enhances brain-derived neurotrophic factor production and neurogenesis in the hippocampus following cerebral global ischemia in mice"}]},{"@id":"https://cir.nii.ac.jp/crid/1360004234327861120","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Oxidative stress–dependent phosphorylation activates ZNRF1 to induce neuronal/axonal degeneration"}]},{"@id":"https://cir.nii.ac.jp/crid/1360004234483519104","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Rat Cranial Bone-Derived Mesenchymal Stem Cell Transplantation Promotes Functional Recovery in Ischemic Stroke Model Rats"}]},{"@id":"https://cir.nii.ac.jp/crid/1360021391857292032","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Role of calpain-5 in cerebral ischemia and reperfusion injury"}]},{"@id":"https://cir.nii.ac.jp/crid/1360283691780417536","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Histamine H3 receptors aggravate cerebral ischaemic injury by histamine-independent mechanisms"}]},{"@id":"https://cir.nii.ac.jp/crid/1360285707367851904","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Spatio-temporal spread of neuronal death after focal photolysis of caged glutamate in neuron/astrocyte co-cultures"}]},{"@id":"https://cir.nii.ac.jp/crid/1360568467112156800","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Cellular mechanisms underlying the rapid depolarization caused by oxygen and glucose deprivation in layer III pyramidal cells of the somatosensory cortex"}]},{"@id":"https://cir.nii.ac.jp/crid/1360584341810484864","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Perivascular macrophages in cerebrovascular diseases"}]},{"@id":"https://cir.nii.ac.jp/crid/1360849943933725952","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Neuroprotective effects of different frequency preconditioning exercise on neuronal apoptosis after focal brain ischemia in rats"}]},{"@id":"https://cir.nii.ac.jp/crid/1360853567618010240","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Anti-apoptotic effects of BDNF-TrkB signaling in the treatment of hemorrhagic stroke"}]},{"@id":"https://cir.nii.ac.jp/crid/1360857593733849856","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Establishing a high throughput drug screening system for cerebral ischemia using zebrafish larvae"}]},{"@id":"https://cir.nii.ac.jp/crid/1360861705602609280","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Novel insights into the mechanism of reactive oxygen species-mediated neurodegeneration"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001205178034688","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Neuroprotective Effect of 4-Methylcyclopentadecanone on Focal Cerebral Ischemia/Reperfusion Injury in Rats"}]},{"@id":"https://cir.nii.ac.jp/crid/1390285697607097344","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Propofol Attenuates Inflammatory Damage <i>via</i> Inhibiting NLRP1-Casp1-Casp6 Signaling in Ischemic Brain Injury"},{"@value":"Propofol Attenuates Inflammatory Damage via Inhibiting NLRP1-Casp1-Casp6 Signaling in Ischemic Brain Injury"}]},{"@id":"https://cir.nii.ac.jp/crid/1390299086444149504","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Epigenetic modification of histone acetylation in the sensorimotor cortex after intracerebral hemorrhage"}]},{"@id":"https://cir.nii.ac.jp/crid/1390570630076539776","@type":"Article","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Retraction: Dexmedetomidine and Phosphocreatine Post-treatment Provides Protection against Focal Cerebral Ischemia-reperfusion Injury in Rats"}]},{"@id":"https://cir.nii.ac.jp/crid/1390855201278705024","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Possible Involvement of DNA Methylation and Protective Effect of Zebularine on Neuronal Cell Death after Glutamate Excitotoxity"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.1161/strokeaha.108.531632"},{"@type":"CROSSREF","@value":"10.1083/jcb.201506102_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"},{"@type":"CROSSREF","@value":"10.1016/j.bbagen.2023.130506_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"},{"@type":"CROSSREF","@value":"10.1038/ncomms4334_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"},{"@type":"CROSSREF","@value":"10.1248/bpb.b20-00050_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"},{"@type":"CROSSREF","@value":"10.1016/j.neuint.2013.03.010_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"},{"@type":"CROSSREF","@value":"10.1248/bpb.b22-00147_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"},{"@type":"CROSSREF","@value":"10.1016/j.neulet.2012.08.079_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"},{"@type":"CROSSREF","@value":"10.1267/ahc.21-00040_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"},{"@type":"CROSSREF","@value":"10.2220/biomedres.45.1_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"},{"@type":"CROSSREF","@value":"10.1016/j.expneurol.2024.114680_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"},{"@type":"CROSSREF","@value":"10.1080/01616412.2019.1580458_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"},{"@type":"CROSSREF","@value":"10.1254/jphs.14102fp_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"},{"@type":"CROSSREF","@value":"10.1016/j.hest.2020.04.003_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"},{"@type":"CROSSREF","@value":"10.1016/j.jphs.2021.06.006_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"},{"@type":"CROSSREF","@value":"10.4103/1673-5374.354509_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"},{"@type":"CROSSREF","@value":"10.1089/scd.2018.0022_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"},{"@type":"CROSSREF","@value":"10.1016/j.neures.2020.03.003_references_DOI_Ms5CODeVaANTcUBJBjWzVl1knmF"}]}