FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2106968981> ?p ?o ?g. }

• W2106968981 endingPage "2338" @default.
• W2106968981 startingPage "2327" @default.
• W2106968981 abstract "Recent investigations have suggested that inflammasome activation plays an important role during atherosclerosis. Upon activation, the inflammasome induces processing and release of pro-inflammatory cytokines interleukin 1β (IL-1β) and interleukin 18 (IL-18) via activation of caspase-1/11. Previously, it was shown that complete caspase-1 deficiency is protective against atherosclerosis development. However, while macrophages are the main inflammatory cells involved in atherosclerosis, the exact role of macrophage-specific caspase-1/11 activation during development of cardiovascular disease has never been investigated. We hypothesized that hematopoietic caspase-1/11 deficiency leads to reduced atherosclerosis development. To investigate the specific contribution of hematopoietic caspase-1/11 activation to atherosclerosis development, Ldlr(-/-) mice received a transplant (tp) of wild-type (WT) or caspase-1/11(-/-) bone marrow, to create WT-tp mice and caspase-1/11(-/-) -tp mice, and fed a high-fat, high-cholesterol diet for 12 weeks. Our results showed an increase in anti-inflammatory blood leukocytes in caspase-1/11(-/-) -tp mice compared with WT-tp mice, as indicated by a decreased level of Ly6C(high) monocytes and an increased level of Ly6C(low) monocytes. In line with our hypothesis, hematopoietic deletion of caspase-1/11 resulted in a strong reduction in atherosclerotic plaque size. Furthermore, necrotic core content was dramatically decreased in caspase-1/11(-/-) -tp mice. Our data indicate that hematopoietic caspase-1/11 activation is involved in vascular inflammation and atherosclerosis, and plays an important role in cardiovascular disease progression." @default.
• W2106968981 created "2016-06-24" @default.
• W2106968981 creator A5002563142 @default.
• W2106968981 creator A5002842593 @default.
• W2106968981 creator A5004706190 @default.
• W2106968981 creator A5020668415 @default.
• W2106968981 creator A5033865421 @default.
• W2106968981 creator A5041576585 @default.
• W2106968981 creator A5049396254 @default.
• W2106968981 creator A5052299049 @default.
• W2106968981 creator A5052509348 @default.
• W2106968981 creator A5082105014 @default.
• W2106968981 creator A5086707368 @default.
• W2106968981 creator A5090059326 @default.
• W2106968981 creator A5090786163 @default.
• W2106968981 date "2015-04-20" @default.
• W2106968981 modified "2023-09-27" @default.
• W2106968981 title "Bone marrow-specific caspase-1/11 deficiency inhibits atherosclerosis development in<i>Ldlr</i>^{<i>−/−</i>}mice" @default.
• W2106968981 cites W1964957913 @default.
• W2106968981 cites W1966650064 @default.
• W2106968981 cites W1966980019 @default.
• W2106968981 cites W1972483153 @default.
• W2106968981 cites W1985942166 @default.
• W2106968981 cites W2002175938 @default.
• W2106968981 cites W2010520310 @default.
• W2106968981 cites W2020154042 @default.
• W2106968981 cites W2022837368 @default.
• W2106968981 cites W2026212701 @default.
• W2106968981 cites W2027922456 @default.
• W2106968981 cites W2028545985 @default.
• W2106968981 cites W2046208657 @default.
• W2106968981 cites W2048827030 @default.
• W2106968981 cites W2052554962 @default.
• W2106968981 cites W2056245899 @default.
• W2106968981 cites W2056888748 @default.
• W2106968981 cites W2078095032 @default.
• W2106968981 cites W2079864944 @default.
• W2106968981 cites W2080827095 @default.
• W2106968981 cites W2082078082 @default.
• W2106968981 cites W2082400315 @default.
• W2106968981 cites W2085611491 @default.
• W2106968981 cites W2100820895 @default.
• W2106968981 cites W2105263387 @default.
• W2106968981 cites W2119863741 @default.
• W2106968981 cites W2129304025 @default.
• W2106968981 cites W2135647797 @default.
• W2106968981 cites W2151401603 @default.
• W2106968981 cites W2153328565 @default.
• W2106968981 cites W2156531013 @default.
• W2106968981 cites W2156593520 @default.
• W2106968981 cites W2158380859 @default.
• W2106968981 cites W2167915346 @default.
• W2106968981 cites W4247956906 @default.
• W2106968981 doi "https://doi.org/10.1111/febs.13279" @default.
• W2106968981 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25817537" @default.
• W2106968981 hasPublicationYear "2015" @default.
• W2106968981 type Work @default.
• W2106968981 sameAs 2106968981 @default.
• W2106968981 citedByCount "60" @default.
• W2106968981 countsByYear W21069689812015 @default.
• W2106968981 countsByYear W21069689812016 @default.
• W2106968981 countsByYear W21069689812017 @default.
• W2106968981 countsByYear W21069689812018 @default.
• W2106968981 countsByYear W21069689812019 @default.
• W2106968981 countsByYear W21069689812020 @default.
• W2106968981 countsByYear W21069689812021 @default.
• W2106968981 countsByYear W21069689812022 @default.
• W2106968981 countsByYear W21069689812023 @default.
• W2106968981 crossrefType "journal-article" @default.
• W2106968981 hasAuthorship W2106968981A5002563142 @default.
• W2106968981 hasAuthorship W2106968981A5002842593 @default.
• W2106968981 hasAuthorship W2106968981A5004706190 @default.
• W2106968981 hasAuthorship W2106968981A5020668415 @default.
• W2106968981 hasAuthorship W2106968981A5033865421 @default.
• W2106968981 hasAuthorship W2106968981A5041576585 @default.
• W2106968981 hasAuthorship W2106968981A5049396254 @default.
• W2106968981 hasAuthorship W2106968981A5052299049 @default.
• W2106968981 hasAuthorship W2106968981A5052509348 @default.
• W2106968981 hasAuthorship W2106968981A5082105014 @default.
• W2106968981 hasAuthorship W2106968981A5086707368 @default.
• W2106968981 hasAuthorship W2106968981A5090059326 @default.
• W2106968981 hasAuthorship W2106968981A5090786163 @default.
• W2106968981 hasBestOaLocation W21069689812 @default.
• W2106968981 hasConcept C109159458 @default.
• W2106968981 hasConcept C126322002 @default.
• W2106968981 hasConcept C134018914 @default.
• W2106968981 hasConcept C139964883 @default.
• W2106968981 hasConcept C185592680 @default.
• W2106968981 hasConcept C202751555 @default.
• W2106968981 hasConcept C203014093 @default.
• W2106968981 hasConcept C2776914184 @default.
• W2106968981 hasConcept C2777209026 @default.
• W2106968981 hasConcept C2779244956 @default.
• W2106968981 hasConcept C2780007613 @default.
• W2106968981 hasConcept C28328180 @default.
• W2106968981 hasConcept C55493867 @default.
• W2106968981 hasConcept C71924100 @default.
• W2106968981 hasConcept C86803240 @default.

• next