Matches in SemOpenAlex for { <https://semopenalex.org/work/W2134733089> ?p ?o ?g. }
Showing items 1 to 76 of
76
with 100 items per page.
- W2134733089 endingPage "205" @default.
- W2134733089 startingPage "193" @default.
- W2134733089 abstract "Glutamate excitotoxicity, oxidative stress, and acidosis are primary mediators of neuronal death during ischemia and reperfusion. Astrocytes influence these processes in several ways. Glutamate uptake by astrocytes normally prevents excitotoxic glutamate elevations in brain extracellular space, and this process appears to be a critical determinant of neuronal survival in the ischemic penumbra. Conversely, glutamate efflux from astrocytes by reversal of glutamate uptake, volume sensitive organic ion channels, and other routes may contribute to extracellular glutamate elevations. Glutamate activation of neuronal N-methyl-D-aspartate (NMDA) receptors is modulated by glycine and D-serine: both of these neuromodulators are transported by astrocytes, and D-serine production is localized exclusively to astrocytes. Astrocytes influence neuronal antioxidant status through release of ascorbate and uptake of its oxidized form, dehydroascorbate, and by indirectly supporting neuronal glutathione metabolism. In addition, glutathione in astrocytes can serve as a sink for nitric oxide and thereby reduce neuronal oxidant stress during ischemia. Astrocytes probably also influence neuronal survival in the post-ischemic period. Reactive astrocytes secrete nitric oxide, TNFalpha, matrix metalloproteinases, and other factors that can contribute to delayed neuronal death, and facilitate brain edema via aquaporin-4 channels localized to the astrocyte endfoot-endothelial interface. On the other hand erythropoietin, a paracrine messenger in brain, is produced by astrocytes and upregulated after ischemia. Erythropoietin stimulates the Janus kinase-2 (JAK-2) and nuclear factor-kappaB (NF-kB) signaling pathways in neurons to prevent programmed cell death after ischemic or excitotoxic stress. Astrocytes also secrete several angiogenic and neurotrophic factors that are important for vascular and neuronal regeneration after stroke." @default.
- W2134733089 created "2016-06-24" @default.
- W2134733089 creator A5017734543 @default.
- W2134733089 creator A5022193976 @default.
- W2134733089 creator A5086512694 @default.
- W2134733089 date "2004-03-01" @default.
- W2134733089 modified "2023-09-29" @default.
- W2134733089 title "Astrocyte Influences on Ischemic Neuronal Death" @default.
- W2134733089 doi "https://doi.org/10.2174/1566524043479185" @default.
- W2134733089 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15032713" @default.
- W2134733089 hasPublicationYear "2004" @default.
- W2134733089 type Work @default.
- W2134733089 sameAs 2134733089 @default.
- W2134733089 citedByCount "406" @default.
- W2134733089 countsByYear W21347330892012 @default.
- W2134733089 countsByYear W21347330892013 @default.
- W2134733089 countsByYear W21347330892014 @default.
- W2134733089 countsByYear W21347330892015 @default.
- W2134733089 countsByYear W21347330892016 @default.
- W2134733089 countsByYear W21347330892017 @default.
- W2134733089 countsByYear W21347330892018 @default.
- W2134733089 countsByYear W21347330892019 @default.
- W2134733089 countsByYear W21347330892020 @default.
- W2134733089 countsByYear W21347330892021 @default.
- W2134733089 countsByYear W21347330892022 @default.
- W2134733089 countsByYear W21347330892023 @default.
- W2134733089 crossrefType "journal-article" @default.
- W2134733089 hasAuthorship W2134733089A5017734543 @default.
- W2134733089 hasAuthorship W2134733089A5022193976 @default.
- W2134733089 hasAuthorship W2134733089A5086512694 @default.
- W2134733089 hasConcept C169760540 @default.
- W2134733089 hasConcept C170493617 @default.
- W2134733089 hasConcept C185592680 @default.
- W2134733089 hasConcept C25498285 @default.
- W2134733089 hasConcept C2777542381 @default.
- W2134733089 hasConcept C2780884517 @default.
- W2134733089 hasConcept C2781012912 @default.
- W2134733089 hasConcept C529278444 @default.
- W2134733089 hasConcept C55493867 @default.
- W2134733089 hasConcept C61174792 @default.
- W2134733089 hasConcept C86803240 @default.
- W2134733089 hasConcept C95444343 @default.
- W2134733089 hasConceptScore W2134733089C169760540 @default.
- W2134733089 hasConceptScore W2134733089C170493617 @default.
- W2134733089 hasConceptScore W2134733089C185592680 @default.
- W2134733089 hasConceptScore W2134733089C25498285 @default.
- W2134733089 hasConceptScore W2134733089C2777542381 @default.
- W2134733089 hasConceptScore W2134733089C2780884517 @default.
- W2134733089 hasConceptScore W2134733089C2781012912 @default.
- W2134733089 hasConceptScore W2134733089C529278444 @default.
- W2134733089 hasConceptScore W2134733089C55493867 @default.
- W2134733089 hasConceptScore W2134733089C61174792 @default.
- W2134733089 hasConceptScore W2134733089C86803240 @default.
- W2134733089 hasConceptScore W2134733089C95444343 @default.
- W2134733089 hasIssue "2" @default.
- W2134733089 hasLocation W21347330891 @default.
- W2134733089 hasLocation W21347330892 @default.
- W2134733089 hasOpenAccess W2134733089 @default.
- W2134733089 hasPrimaryLocation W21347330891 @default.
- W2134733089 hasRelatedWork W1995963726 @default.
- W2134733089 hasRelatedWork W2012584819 @default.
- W2134733089 hasRelatedWork W2028368650 @default.
- W2134733089 hasRelatedWork W2047245618 @default.
- W2134733089 hasRelatedWork W2070004275 @default.
- W2134733089 hasRelatedWork W2090832170 @default.
- W2134733089 hasRelatedWork W2090937429 @default.
- W2134733089 hasRelatedWork W2111343607 @default.
- W2134733089 hasRelatedWork W2168571869 @default.
- W2134733089 hasRelatedWork W3031787350 @default.
- W2134733089 hasVolume "4" @default.
- W2134733089 isParatext "false" @default.
- W2134733089 isRetracted "false" @default.
- W2134733089 magId "2134733089" @default.
- W2134733089 workType "article" @default.