FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4320710159> ?p ?o ?g. }

• W4320710159 endingPage "722" @default.
• W4320710159 startingPage "707" @default.
• W4320710159 abstract "Background: Cardiac remodeling in heart failure involves macrophage-mediated immune responses. Recent studies have shown that a PRR (pattern recognition receptor) called dectin-1, expressed on macrophages, mediates proinflammatory responses. Whether dectin-1 plays a role in pathological cardiac remodeling is unknown. Here, we identified a potential role of dectin-1 in this disease. Methods: To model aberrant cardiac remodeling, we utilized mouse models of chronic Ang II (angiotensin II) infusion. In this model, we assessed the potential role of dectin-1 through using D1KO (dectin-1 knockout) mice and bone marrow transplantation chimeric mice. We then used cellular and molecular assays to discover the underlying mechanisms of dectin-1 function. Results: We found that macrophage dectin-1 is elevated in mouse heart tissues following chronic Ang II administration. D1KO mice were significantly protected against Ang II–induced cardiac dysfunction, hypertrophy, fibrosis, inflammatory responses, and macrophage infiltration. Further bone marrow transplantation studies showed that dectin-1 deficiency in bone marrow–derived cells prevented Ang II–induced cardiac inflammation and dysfunction. Through detailed molecular studies, we show that Ang II binds directly to dectin-1, causing dectin-1 homodimerization and activating the downstream Syk (spleen tyrosine kinase)/NF-κB (nuclear factor kappa B) signaling pathway to induce expression of inflammatory and chemoattractant factors. Mutagenesis studies identified R184 in the C-type lectin domain to interact with Ang II. Blocking dectin-1 in macrophages suppresses Ang II–induced inflammatory mediators and subsequent intercellular cross talk with cardiomyocytes and fibroblasts. Conclusions: Our study has discovered dectin-1 as a new nonclassical receptor of Ang II and a key player in cardiac remolding and dysfunction. These studies suggest that dectin-1 may be a new target for treating hypertension-related heart failure." @default.
• W4320710159 created "2023-02-15" @default.
• W4320710159 creator A5007721967 @default.
• W4320710159 creator A5007767899 @default.
• W4320710159 creator A5010180547 @default.
• W4320710159 creator A5010526490 @default.
• W4320710159 creator A5019472642 @default.
• W4320710159 creator A5019486303 @default.
• W4320710159 creator A5024555543 @default.
• W4320710159 creator A5029667848 @default.
• W4320710159 creator A5041664447 @default.
• W4320710159 creator A5053579924 @default.
• W4320710159 creator A5074286511 @default.
• W4320710159 creator A5077232265 @default.
• W4320710159 creator A5088131716 @default.
• W4320710159 date "2023-03-17" @default.
• W4320710159 modified "2023-10-14" @default.
• W4320710159 title "Dectin-1 Acts as a Non-Classical Receptor of Ang II to Induce Cardiac Remodeling" @default.
• W4320710159 cites W1963606632 @default.
• W4320710159 cites W1973425514 @default.
• W4320710159 cites W1976925504 @default.
• W4320710159 cites W2004336750 @default.
• W4320710159 cites W2058258787 @default.
• W4320710159 cites W2066222426 @default.
• W4320710159 cites W2103325328 @default.
• W4320710159 cites W2105668062 @default.
• W4320710159 cites W2126009588 @default.
• W4320710159 cites W2134213199 @default.
• W4320710159 cites W2136714451 @default.
• W4320710159 cites W2140333814 @default.
• W4320710159 cites W2147406541 @default.
• W4320710159 cites W2154360613 @default.
• W4320710159 cites W2157944478 @default.
• W4320710159 cites W2170533080 @default.
• W4320710159 cites W2170533815 @default.
• W4320710159 cites W2179410813 @default.
• W4320710159 cites W2378919362 @default.
• W4320710159 cites W2414866219 @default.
• W4320710159 cites W2470581182 @default.
• W4320710159 cites W2565989841 @default.
• W4320710159 cites W2594483928 @default.
• W4320710159 cites W2605540758 @default.
• W4320710159 cites W2705866519 @default.
• W4320710159 cites W2737901609 @default.
• W4320710159 cites W2791059232 @default.
• W4320710159 cites W2792454313 @default.
• W4320710159 cites W2803875087 @default.
• W4320710159 cites W2806295635 @default.
• W4320710159 cites W2894273957 @default.
• W4320710159 cites W2947872410 @default.
• W4320710159 cites W2964593755 @default.
• W4320710159 cites W2979176820 @default.
• W4320710159 cites W2982287350 @default.
• W4320710159 cites W2982367920 @default.
• W4320710159 cites W2992634090 @default.
• W4320710159 cites W3043135743 @default.
• W4320710159 cites W3113997264 @default.
• W4320710159 cites W3127530509 @default.
• W4320710159 cites W3128212022 @default.
• W4320710159 cites W3131501316 @default.
• W4320710159 cites W3148433444 @default.
• W4320710159 cites W3184722892 @default.
• W4320710159 cites W3193598686 @default.
• W4320710159 cites W3194068824 @default.
• W4320710159 cites W3195284485 @default.
• W4320710159 cites W3197958064 @default.
• W4320710159 cites W3211998458 @default.
• W4320710159 doi "https://doi.org/10.1161/circresaha.122.322259" @default.
• W4320710159 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36786193" @default.
• W4320710159 hasPublicationYear "2023" @default.
• W4320710159 type Work @default.
• W4320710159 citedByCount "3" @default.
• W4320710159 countsByYear W43207101592023 @default.
• W4320710159 crossrefType "journal-article" @default.
• W4320710159 hasAuthorship W4320710159A5007721967 @default.
• W4320710159 hasAuthorship W4320710159A5007767899 @default.
• W4320710159 hasAuthorship W4320710159A5010180547 @default.
• W4320710159 hasAuthorship W4320710159A5010526490 @default.
• W4320710159 hasAuthorship W4320710159A5019472642 @default.
• W4320710159 hasAuthorship W4320710159A5019486303 @default.
• W4320710159 hasAuthorship W4320710159A5024555543 @default.
• W4320710159 hasAuthorship W4320710159A5029667848 @default.
• W4320710159 hasAuthorship W4320710159A5041664447 @default.
• W4320710159 hasAuthorship W4320710159A5053579924 @default.
• W4320710159 hasAuthorship W4320710159A5074286511 @default.
• W4320710159 hasAuthorship W4320710159A5077232265 @default.
• W4320710159 hasAuthorship W4320710159A5088131716 @default.
• W4320710159 hasConcept C126322002 @default.
• W4320710159 hasConcept C164027704 @default.
• W4320710159 hasConcept C170493617 @default.
• W4320710159 hasConcept C202751555 @default.
• W4320710159 hasConcept C203014093 @default.
• W4320710159 hasConcept C2776914184 @default.
• W4320710159 hasConcept C2777420927 @default.
• W4320710159 hasConcept C2779244956 @default.
• W4320710159 hasConcept C2780559512 @default.
• W4320710159 hasConcept C2908929049 @default.
• W4320710159 hasConcept C502942594 @default.

• next