FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2129304025> ?p ?o ?g. }

• W2129304025 endingPage "e78792" @default.
• W2129304025 startingPage "e78792" @default.
• W2129304025 abstract "While non-alcoholic steatohepatitis (NASH) is characterized by hepatic steatosis combined with inflammation, the mechanisms triggering hepatic inflammation are unknown. In Ldlr(-/-) mice, we have previously shown that lysosomal cholesterol accumulation in Kupffer cells (KCs) correlates with hepatic inflammation and cholesterol crystallization. Previously, cholesterol crystals have been shown to induce the activation of inflammasomes. Inflammasomes are protein complexes that induce the processing and release of pro-inflammatory cytokines IL-1b and IL-18 via caspase-1 activation. Whereas caspase-1 activation is independent of caspase-11 in the canonical pathway of inflammasome activation, caspase-11 was found to trigger caspase-1-dependent IL-1b and IL-18 in response to non-canonical inflammasome activators. So far, it has not been investigated whether inflammasome activation stimulates the formation of cholesterol crystals. We hypothesized that inflammasome activation in KCs stimulates cholesterol crystallization, thereby leading to hepatic inflammation.Ldlr (-/-) mice were transplanted (tp) with wild-type (Wt) or caspase-1/11(-/-) (dKO) bone marrow and fed either regular chow or a high-fat, high-cholesterol (HFC) diet for 12 weeks. In vitro, bone marrow derived macrophages (BMDM) from wt or caspase-1/11(-/-) mice were incubated with oxLDL for 24h and autophagy was assessed.In line with our hypothesis, caspase-1/11(-/-)-tp mice had less severe hepatic inflammation than Wt-tp animals, as evident from liver histology and gene expression analysis in isolated KCs. Mechanistically, KCs from caspase-1/11(-/-)-tp mice showed less cholesterol crystals, enhanced cholesterol efflux and increased autophagy. In wt BMDM, oxLDL incubation led to disturbed autophagy activity whereas BMDM from caspase-1/11(-/-) mice had normal autophagy activity.Altogether, these data suggest a vicious cycle whereby disturbed autophagy and decreased cholesterol efflux leads to newly formed cholesterol crystals and thereby maintain hepatic inflammation during NASH by further activating the inflammasome." @default.
• W2129304025 created "2016-06-24" @default.
• W2129304025 creator A5002755181 @default.
• W2129304025 creator A5002842593 @default.
• W2129304025 creator A5004706190 @default.
• W2129304025 creator A5027955775 @default.
• W2129304025 creator A5033865421 @default.
• W2129304025 creator A5036411537 @default.
• W2129304025 creator A5037635862 @default.
• W2129304025 creator A5045331825 @default.
• W2129304025 creator A5052509348 @default.
• W2129304025 creator A5063740703 @default.
• W2129304025 creator A5082105014 @default.
• W2129304025 creator A5082220990 @default.
• W2129304025 creator A5086707368 @default.
• W2129304025 creator A5090786163 @default.
• W2129304025 date "2013-12-02" @default.
• W2129304025 modified "2023-10-03" @default.
• W2129304025 title "Macrophage Specific Caspase-1/11 Deficiency Protects against Cholesterol Crystallization and Hepatic Inflammation in Hyperlipidemic Mice" @default.
• W2129304025 cites W1529674879 @default.
• W2129304025 cites W1964844389 @default.
• W2129304025 cites W1966650064 @default.
• W2129304025 cites W1972483153 @default.
• W2129304025 cites W1983619827 @default.
• W2129304025 cites W1988747541 @default.
• W2129304025 cites W1992359197 @default.
• W2129304025 cites W1995781465 @default.
• W2129304025 cites W2007505836 @default.
• W2129304025 cites W2008580473 @default.
• W2129304025 cites W2010520310 @default.
• W2129304025 cites W2028545985 @default.
• W2129304025 cites W2037555606 @default.
• W2129304025 cites W2042767581 @default.
• W2129304025 cites W2045531934 @default.
• W2129304025 cites W2048032544 @default.
• W2129304025 cites W2056888748 @default.
• W2129304025 cites W2059566565 @default.
• W2129304025 cites W2064741210 @default.
• W2129304025 cites W2076062022 @default.
• W2129304025 cites W2080827095 @default.
• W2129304025 cites W2082078082 @default.
• W2129304025 cites W2084589154 @default.
• W2129304025 cites W2087616650 @default.
• W2129304025 cites W2088170171 @default.
• W2129304025 cites W2105263387 @default.
• W2129304025 cites W2107716725 @default.
• W2129304025 cites W2109716633 @default.
• W2129304025 cites W2119098586 @default.
• W2129304025 cites W2119863741 @default.
• W2129304025 cites W2122623396 @default.
• W2129304025 cites W2126384811 @default.
• W2129304025 cites W2128738849 @default.
• W2129304025 cites W2135450217 @default.
• W2129304025 cites W2135574023 @default.
• W2129304025 cites W2137573856 @default.
• W2129304025 cites W2139285220 @default.
• W2129304025 cites W2139776835 @default.
• W2129304025 cites W2144275312 @default.
• W2129304025 cites W2151401603 @default.
• W2129304025 cites W2156531013 @default.
• W2129304025 cites W2158630697 @default.
• W2129304025 cites W2159042370 @default.
• W2129304025 cites W2167117819 @default.
• W2129304025 doi "https://doi.org/10.1371/journal.pone.0078792" @default.
• W2129304025 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3846469" @default.
• W2129304025 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24312444" @default.
• W2129304025 hasPublicationYear "2013" @default.
• W2129304025 type Work @default.
• W2129304025 sameAs 2129304025 @default.
• W2129304025 citedByCount "31" @default.
• W2129304025 countsByYear W21293040252014 @default.
• W2129304025 countsByYear W21293040252015 @default.
• W2129304025 countsByYear W21293040252016 @default.
• W2129304025 countsByYear W21293040252017 @default.
• W2129304025 countsByYear W21293040252018 @default.
• W2129304025 countsByYear W21293040252020 @default.
• W2129304025 countsByYear W21293040252021 @default.
• W2129304025 countsByYear W21293040252022 @default.
• W2129304025 countsByYear W21293040252023 @default.
• W2129304025 crossrefType "journal-article" @default.
• W2129304025 hasAuthorship W2129304025A5002755181 @default.
• W2129304025 hasAuthorship W2129304025A5002842593 @default.
• W2129304025 hasAuthorship W2129304025A5004706190 @default.
• W2129304025 hasAuthorship W2129304025A5027955775 @default.
• W2129304025 hasAuthorship W2129304025A5033865421 @default.
• W2129304025 hasAuthorship W2129304025A5036411537 @default.
• W2129304025 hasAuthorship W2129304025A5037635862 @default.
• W2129304025 hasAuthorship W2129304025A5045331825 @default.
• W2129304025 hasAuthorship W2129304025A5052509348 @default.
• W2129304025 hasAuthorship W2129304025A5063740703 @default.
• W2129304025 hasAuthorship W2129304025A5082105014 @default.
• W2129304025 hasAuthorship W2129304025A5082220990 @default.
• W2129304025 hasAuthorship W2129304025A5086707368 @default.
• W2129304025 hasAuthorship W2129304025A5090786163 @default.
• W2129304025 hasBestOaLocation W21293040251 @default.
• W2129304025 hasConcept C104317684 @default.
• W2129304025 hasConcept C126322002 @default.
• W2129304025 hasConcept C134018914 @default.

• next