FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2789237792> ?p ?o ?g. }

• W2789237792 endingPage "1674" @default.
• W2789237792 startingPage "1663" @default.
• W2789237792 abstract "Acute lung injury (ALI) is one of several complications in patients with traumatic brain injury (TBI). Autophagy is a primary homeostatic process that promotes cell survival under stress. Accumulating evidence implicates autophagy in the pathogenesis of ALI under various conditions. However, the role of autophagy in TBI-induced ALI remains unknown. The aim of this study was to adjust autophagy with pharmacological agents to determine its functional significance in TBI-induced ALI. Rats were preconditioned with autophagy promoter rapamycin or inhibitor 3-methyladenine before they were challenged with TBI. Extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitor U0126, mechanistic target of rapamycin (mTOR) inhibitor rapamycin, and signal transducer and activator of transcription 3 (Stat3) inhibitor S31-201 were used to test the role of ERK1/2/mTOR/Stat3 signaling pathway in regulating autophagy. Autophagy is activated in lung tissues after TBI. Enhancement of autophagy suppressed apoptosis, inflammation and oxidative stress in lung tissues, which were activated after TBI, whereas inhibition of autophagy aggravated these critical pathological changes. Autophagy also improved TBI-induced impairment in pulmonary barrier function, oxygenation function and static compliance. Furthermore, TBI-induced autophagy was mediated by ERK1/2/mTOR/Stat3 pathway, which may serve to reduce ALI and improve pulmonary barrier function, oxygenation function and static compliance. These findings are important for the prevention and treatment of TBI-induced ALI. • Autophagy flux is activated in lung tissues in a rat TBI model. • Autophagy plays a protective role against TBI-induced ALI. • Autophagy suppresses apoptosis, inflammation and oxidative stress in lung tissues after TBI. • TBI-induced autophagy is mediated by ERK1/2/mTOR/Stat3 signaling pathway." @default.
• W2789237792 created "2018-03-29" @default.
• W2789237792 creator A5013630392 @default.
• W2789237792 creator A5020034543 @default.
• W2789237792 creator A5023739579 @default.
• W2789237792 creator A5024180269 @default.
• W2789237792 creator A5046454314 @default.
• W2789237792 creator A5053692207 @default.
• W2789237792 creator A5060335470 @default.
• W2789237792 creator A5072965837 @default.
• W2789237792 creator A5074408964 @default.
• W2789237792 creator A5074571144 @default.
• W2789237792 creator A5075649099 @default.
• W2789237792 date "2018-05-01" @default.
• W2789237792 modified "2023-10-12" @default.
• W2789237792 title "ERK1/2/mTOR/Stat3 pathway-mediated autophagy alleviates traumatic brain injury-induced acute lung injury" @default.
• W2789237792 cites W1491455993 @default.
• W2789237792 cites W1494447887 @default.
• W2789237792 cites W1924919685 @default.
• W2789237792 cites W1928848518 @default.
• W2789237792 cites W1965434923 @default.
• W2789237792 cites W1965995518 @default.
• W2789237792 cites W1966710684 @default.
• W2789237792 cites W1969770915 @default.
• W2789237792 cites W1971046557 @default.
• W2789237792 cites W1990819855 @default.
• W2789237792 cites W1990934962 @default.
• W2789237792 cites W1991688383 @default.
• W2789237792 cites W1996818135 @default.
• W2789237792 cites W2005002911 @default.
• W2789237792 cites W2017280299 @default.
• W2789237792 cites W2018252938 @default.
• W2789237792 cites W2018789868 @default.
• W2789237792 cites W2019576484 @default.
• W2789237792 cites W2021049193 @default.
• W2789237792 cites W2025332003 @default.
• W2789237792 cites W2038559524 @default.
• W2789237792 cites W2085950149 @default.
• W2789237792 cites W2095157531 @default.
• W2789237792 cites W2105111481 @default.
• W2789237792 cites W2109095930 @default.
• W2789237792 cites W2127176298 @default.
• W2789237792 cites W2127761382 @default.
• W2789237792 cites W2132027478 @default.
• W2789237792 cites W2148701132 @default.
• W2789237792 cites W2150279416 @default.
• W2789237792 cites W2152977980 @default.
• W2789237792 cites W2156284838 @default.
• W2789237792 cites W2240173075 @default.
• W2789237792 cites W2268048446 @default.
• W2789237792 cites W2313054568 @default.
• W2789237792 cites W2341322661 @default.
• W2789237792 cites W2398350959 @default.
• W2789237792 cites W2403623483 @default.
• W2789237792 cites W2414526879 @default.
• W2789237792 cites W2505024819 @default.
• W2789237792 cites W2509308857 @default.
• W2789237792 cites W2510013939 @default.
• W2789237792 cites W2523712370 @default.
• W2789237792 cites W2536572117 @default.
• W2789237792 cites W2549235342 @default.
• W2789237792 cites W2568166803 @default.
• W2789237792 cites W2594772834 @default.
• W2789237792 cites W4293384371 @default.
• W2789237792 doi "https://doi.org/10.1016/j.bbadis.2018.02.011" @default.
• W2789237792 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29466698" @default.
• W2789237792 hasPublicationYear "2018" @default.
• W2789237792 type Work @default.
• W2789237792 sameAs 2789237792 @default.
• W2789237792 citedByCount "32" @default.
• W2789237792 countsByYear W27892377922018 @default.
• W2789237792 countsByYear W27892377922019 @default.
• W2789237792 countsByYear W27892377922020 @default.
• W2789237792 countsByYear W27892377922021 @default.
• W2789237792 countsByYear W27892377922022 @default.
• W2789237792 countsByYear W27892377922023 @default.
• W2789237792 crossrefType "journal-article" @default.
• W2789237792 hasAuthorship W2789237792A5013630392 @default.
• W2789237792 hasAuthorship W2789237792A5020034543 @default.
• W2789237792 hasAuthorship W2789237792A5023739579 @default.
• W2789237792 hasAuthorship W2789237792A5024180269 @default.
• W2789237792 hasAuthorship W2789237792A5046454314 @default.
• W2789237792 hasAuthorship W2789237792A5053692207 @default.
• W2789237792 hasAuthorship W2789237792A5060335470 @default.
• W2789237792 hasAuthorship W2789237792A5072965837 @default.
• W2789237792 hasAuthorship W2789237792A5074408964 @default.
• W2789237792 hasAuthorship W2789237792A5074571144 @default.
• W2789237792 hasAuthorship W2789237792A5075649099 @default.
• W2789237792 hasConcept C126322002 @default.
• W2789237792 hasConcept C190283241 @default.
• W2789237792 hasConcept C203014093 @default.
• W2789237792 hasConcept C203522944 @default.
• W2789237792 hasConcept C2776151105 @default.
• W2789237792 hasConcept C2776914184 @default.
• W2789237792 hasConcept C2778923194 @default.
• W2789237792 hasConcept C502942594 @default.
• W2789237792 hasConcept C55493867 @default.
• W2789237792 hasConcept C62478195 @default.

• next