Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2003-12-11
pubmed:abstractText
Neurons subjected to ischemia undergo necrosis or apoptosis depending on their anatomic distribution and the severity and duration of ischemia. Recent work has shown that apoptosis can occur in some settings, primarily within the ischemic penumbra. It is recognized that both mitochondrial and death-receptor pathways are involved in the transduction of apoptotic signals in the context of cerebral ischemia. Recent data also highlight the pivotal role of caspase 3 in the execution of ischemia-induced apoptosis, although a caspase-independent pathway is gaining increasing attention. In this review, we examine some of these findings and their potential therapeutic implications for ischemic stroke.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0214-0934
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
497-503
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Cellular and molecular events underlying ischemia-induced neuronal apoptosis.
pubmed:affiliation
Department of Neurosurgery, Stanford University School of Medicine, Stanford, California 94305, USA. yenari@alum.mit.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review