FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2942419033> ?p ?o ?g. }

• W2942419033 endingPage "14779" @default.
• W2942419033 startingPage "14771" @default.
• W2942419033 abstract "Cerebral ischemia/reperfusion (I/R) typically occurs after mechanical thrombectomy to treat ischemic stroke, generation of reactive oxygen species (ROS) after reperfusion may result in neuronal insult, ultimately leading to disability and death. Regulated in development and DNA damage responses 1 (REDD1) is a conserved stress response protein under various pathogenic conditions. Recent research confirms the controversial role of REDD1 in injury processes. Nevertheless, the role of REDD1 in cerebral I/R remains poorly defined. In the current study, increased expression of REDD1 was observed in neurons exposed to simulated I/R via oxygen glucose deprivation/reoxygenation (OGD/R) treatment. Knockdown of REDD1 enhanced OGD/R-inhibited cell viability, but suppressed lactate dehydrogenase (LDH) release in neurons upon OGD/R. Simultaneously, suppression of REDD1 also antagonized OGD/R-evoked cell apoptosis, Bax expression, and caspase-3 activity. Intriguingly, REDD1 depression abrogated neuronal oxidative stress under OGD/R condition by suppressing ROS, MDA generation, and increasing antioxidant SOD levels. Further mechanism analysis corroborated the excessive activation of autophagy in neurons upon OGD/R with increased expression of autophagy-related LC3 and Beclin-1, but decreased autophagy substrate p62 expression. Notably, REDD1 inhibition reversed OGD/R-triggered excessive neuronal autophagy. More importantly, depression of REDD1 also elevated the expression of p-mTOR. Preconditioning with mTOR inhibitor rapamycin engendered not only a reduction in mTOR activation, but also a reactivation of autophagy in REDD1 knockdown-neurons upon OGD/R. In addition, blocking the mTOR pathway muted the protective roles of REDD1 inhibition against OGD/R-induced neuron injury and oxidative stress. Together these data suggested that REDD1 may regulate I/R-induced oxidative stress injury in neurons by mediating mTOR-autophagy signaling, supporting a promising therapeutic strategy against brain ischemic diseases." @default.
• W2942419033 created "2019-05-03" @default.
• W2942419033 creator A5024923608 @default.
• W2942419033 creator A5048324020 @default.
• W2942419033 date "2019-04-25" @default.
• W2942419033 modified "2023-10-01" @default.
• W2942419033 title "Suppression of REDD1 attenuates oxygen glucose deprivation/reoxygenation‐evoked ischemic injury in neuron by suppressing mTOR‐mediated excessive autophagy" @default.
• W2942419033 cites W1970188265 @default.
• W2942419033 cites W1980026775 @default.
• W2942419033 cites W2020730169 @default.
• W2942419033 cites W2026500101 @default.
• W2942419033 cites W2042515284 @default.
• W2942419033 cites W2092429129 @default.
• W2942419033 cites W2113928060 @default.
• W2942419033 cites W2144827275 @default.
• W2942419033 cites W2251136725 @default.
• W2942419033 cites W2264222646 @default.
• W2942419033 cites W2277050883 @default.
• W2942419033 cites W2300808435 @default.
• W2942419033 cites W2338986048 @default.
• W2942419033 cites W2403483921 @default.
• W2942419033 cites W2403955714 @default.
• W2942419033 cites W2623490112 @default.
• W2942419033 cites W2725092383 @default.
• W2942419033 cites W2728597713 @default.
• W2942419033 cites W2738260606 @default.
• W2942419033 cites W2765644979 @default.
• W2942419033 cites W2766212588 @default.
• W2942419033 cites W2766517326 @default.
• W2942419033 cites W2796430156 @default.
• W2942419033 cites W2797306797 @default.
• W2942419033 cites W2799334490 @default.
• W2942419033 cites W2800016136 @default.
• W2942419033 cites W2802112449 @default.
• W2942419033 cites W2808593337 @default.
• W2942419033 cites W2808836679 @default.
• W2942419033 cites W567021032 @default.
• W2942419033 doi "https://doi.org/10.1002/jcb.28737" @default.
• W2942419033 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31021470" @default.
• W2942419033 hasPublicationYear "2019" @default.
• W2942419033 type Work @default.
• W2942419033 sameAs 2942419033 @default.
• W2942419033 citedByCount "23" @default.
• W2942419033 countsByYear W29424190332019 @default.
• W2942419033 countsByYear W29424190332020 @default.
• W2942419033 countsByYear W29424190332021 @default.
• W2942419033 countsByYear W29424190332022 @default.
• W2942419033 countsByYear W29424190332023 @default.
• W2942419033 crossrefType "journal-article" @default.
• W2942419033 hasAuthorship W2942419033A5024923608 @default.
• W2942419033 hasAuthorship W2942419033A5048324020 @default.
• W2942419033 hasConcept C126322002 @default.
• W2942419033 hasConcept C173396325 @default.
• W2942419033 hasConcept C185592680 @default.
• W2942419033 hasConcept C190283241 @default.
• W2942419033 hasConcept C203522944 @default.
• W2942419033 hasConcept C25498285 @default.
• W2942419033 hasConcept C2776151105 @default.
• W2942419033 hasConcept C2780114680 @default.
• W2942419033 hasConcept C31573885 @default.
• W2942419033 hasConcept C48349386 @default.
• W2942419033 hasConcept C541997718 @default.
• W2942419033 hasConcept C55493867 @default.
• W2942419033 hasConcept C71924100 @default.
• W2942419033 hasConcept C86554907 @default.
• W2942419033 hasConcept C86803240 @default.
• W2942419033 hasConcept C95444343 @default.
• W2942419033 hasConcept C98274493 @default.
• W2942419033 hasConceptScore W2942419033C126322002 @default.
• W2942419033 hasConceptScore W2942419033C173396325 @default.
• W2942419033 hasConceptScore W2942419033C185592680 @default.
• W2942419033 hasConceptScore W2942419033C190283241 @default.
• W2942419033 hasConceptScore W2942419033C203522944 @default.
• W2942419033 hasConceptScore W2942419033C25498285 @default.
• W2942419033 hasConceptScore W2942419033C2776151105 @default.
• W2942419033 hasConceptScore W2942419033C2780114680 @default.
• W2942419033 hasConceptScore W2942419033C31573885 @default.
• W2942419033 hasConceptScore W2942419033C48349386 @default.
• W2942419033 hasConceptScore W2942419033C541997718 @default.
• W2942419033 hasConceptScore W2942419033C55493867 @default.
• W2942419033 hasConceptScore W2942419033C71924100 @default.
• W2942419033 hasConceptScore W2942419033C86554907 @default.
• W2942419033 hasConceptScore W2942419033C86803240 @default.
• W2942419033 hasConceptScore W2942419033C95444343 @default.
• W2942419033 hasConceptScore W2942419033C98274493 @default.
• W2942419033 hasIssue "9" @default.
• W2942419033 hasLocation W29424190331 @default.
• W2942419033 hasLocation W29424190332 @default.
• W2942419033 hasOpenAccess W2942419033 @default.
• W2942419033 hasPrimaryLocation W29424190331 @default.
• W2942419033 hasRelatedWork W2000132737 @default.
• W2942419033 hasRelatedWork W2012224340 @default.
• W2942419033 hasRelatedWork W2035477351 @default.
• W2942419033 hasRelatedWork W2084880710 @default.
• W2942419033 hasRelatedWork W2355246966 @default.
• W2942419033 hasRelatedWork W2890156259 @default.
• W2942419033 hasRelatedWork W2993499003 @default.
• W2942419033 hasRelatedWork W3002644491 @default.

• next