FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3215429829> ?p ?o ?g. }

• W3215429829 endingPage "2984" @default.
• W3215429829 startingPage "2973" @default.
• W3215429829 abstract "Abstract Aims Microvascular inflammation plays an important role in the pathogenesis of diastolic dysfunction (DD) and metabolic heart disease. NOX1 is expressed in vascular and immune cells and has been implicated in the vascular pathology of metabolic disease. However, its contribution to metabolic heart disease is less understood. Methods and results NOX1-deficient mice (KO) and male wild-type (WT) littermates were fed a high-fat high-sucrose diet (HFHS) and injected streptozotocin (75 mg/kg i.p.) or control diet (CTD) and sodium citrate. Despite similar weight gain and increase in fasting blood glucose and insulin, only WT-HFHS but not KO-HFHS mice developed concentric cardiac hypertrophy and elevated left ventricular filling pressure. This was associated with increased endothelial adhesion molecule expression, accumulation of Mac-2-, IL-1β-, and NLRP3-positive cells and nitrosative stress in WT-HFHS but not KO-HFHS hearts. Nox1 mRNA was solidly expressed in CD45+ immune cells isolated from healthy mouse hearts but was negligible in cardiac CD31+ endothelial cells. However, in vitro, Nox1 expression increased in response to lipopolysaccharide (LPS) in endothelial cells and contributed to LPS-induced upregulation of Icam-1. Nox1 was also upregulated in mouse bone marrow-derived macrophages in response to LPS. In peripheral monocytes from age- and sex-matched symptomatic patients with and without DD, NOX1 was significantly higher in patients with DD compared to those without DD. Conclusions NOX1 mediates endothelial activation and contributes to myocardial inflammation and remodelling in metabolic disease in mice. Given its high expression in monocytes of humans with DD, NOX1 may represent a potential target to mitigate heart disease associated with DD." @default.
• W3215429829 created "2021-12-06" @default.
• W3215429829 creator A5008126022 @default.
• W3215429829 creator A5011588479 @default.
• W3215429829 creator A5013827938 @default.
• W3215429829 creator A5014900345 @default.
• W3215429829 creator A5028417593 @default.
• W3215429829 creator A5041928740 @default.
• W3215429829 creator A5047291266 @default.
• W3215429829 creator A5057971415 @default.
• W3215429829 creator A5062416501 @default.
• W3215429829 creator A5065724319 @default.
• W3215429829 creator A5081229617 @default.
• W3215429829 creator A5082085568 @default.
• W3215429829 creator A5084509185 @default.
• W3215429829 creator A5090560496 @default.
• W3215429829 date "2021-11-26" @default.
• W3215429829 modified "2023-10-12" @default.
• W3215429829 title "NOX1 mediates metabolic heart disease in mice and is upregulated in monocytes of humans with diastolic dysfunction" @default.
• W3215429829 cites W164205712 @default.
• W3215429829 cites W1977185778 @default.
• W3215429829 cites W1988293824 @default.
• W3215429829 cites W1994365742 @default.
• W3215429829 cites W2007671598 @default.
• W3215429829 cites W2008411455 @default.
• W3215429829 cites W2009004909 @default.
• W3215429829 cites W2009403275 @default.
• W3215429829 cites W2010484682 @default.
• W3215429829 cites W2026685522 @default.
• W3215429829 cites W2032456441 @default.
• W3215429829 cites W2037572308 @default.
• W3215429829 cites W2053963810 @default.
• W3215429829 cites W2066000449 @default.
• W3215429829 cites W2070647639 @default.
• W3215429829 cites W2085128107 @default.
• W3215429829 cites W2093518775 @default.
• W3215429829 cites W2101745219 @default.
• W3215429829 cites W2119406485 @default.
• W3215429829 cites W2122465146 @default.
• W3215429829 cites W2123617367 @default.
• W3215429829 cites W2137012624 @default.
• W3215429829 cites W2145898095 @default.
• W3215429829 cites W2155084220 @default.
• W3215429829 cites W2157684603 @default.
• W3215429829 cites W2160571418 @default.
• W3215429829 cites W2165604976 @default.
• W3215429829 cites W2166564743 @default.
• W3215429829 cites W2192643629 @default.
• W3215429829 cites W2306006469 @default.
• W3215429829 cites W2335788856 @default.
• W3215429829 cites W2427094903 @default.
• W3215429829 cites W2461909749 @default.
• W3215429829 cites W2501174056 @default.
• W3215429829 cites W2528654783 @default.
• W3215429829 cites W2530814271 @default.
• W3215429829 cites W2547446918 @default.
• W3215429829 cites W2552545260 @default.
• W3215429829 cites W2610719842 @default.
• W3215429829 cites W2620406790 @default.
• W3215429829 cites W2734060625 @default.
• W3215429829 cites W2767058951 @default.
• W3215429829 cites W2779679995 @default.
• W3215429829 cites W2900859474 @default.
• W3215429829 cites W2902050841 @default.
• W3215429829 cites W2902330407 @default.
• W3215429829 cites W2962611490 @default.
• W3215429829 cites W2971111962 @default.
• W3215429829 cites W2972881652 @default.
• W3215429829 cites W3007896475 @default.
• W3215429829 cites W3036835622 @default.
• W3215429829 doi "https://doi.org/10.1093/cvr/cvab349" @default.
• W3215429829 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34849611" @default.
• W3215429829 hasPublicationYear "2021" @default.
• W3215429829 type Work @default.
• W3215429829 sameAs 3215429829 @default.
• W3215429829 citedByCount "9" @default.
• W3215429829 countsByYear W32154298292022 @default.
• W3215429829 countsByYear W32154298292023 @default.
• W3215429829 crossrefType "journal-article" @default.
• W3215429829 hasAuthorship W3215429829A5008126022 @default.
• W3215429829 hasAuthorship W3215429829A5011588479 @default.
• W3215429829 hasAuthorship W3215429829A5013827938 @default.
• W3215429829 hasAuthorship W3215429829A5014900345 @default.
• W3215429829 hasAuthorship W3215429829A5028417593 @default.
• W3215429829 hasAuthorship W3215429829A5041928740 @default.
• W3215429829 hasAuthorship W3215429829A5047291266 @default.
• W3215429829 hasAuthorship W3215429829A5057971415 @default.
• W3215429829 hasAuthorship W3215429829A5062416501 @default.
• W3215429829 hasAuthorship W3215429829A5065724319 @default.
• W3215429829 hasAuthorship W3215429829A5081229617 @default.
• W3215429829 hasAuthorship W3215429829A5082085568 @default.
• W3215429829 hasAuthorship W3215429829A5084509185 @default.
• W3215429829 hasAuthorship W3215429829A5090560496 @default.
• W3215429829 hasBestOaLocation W32154298291 @default.
• W3215429829 hasConcept C104317684 @default.
• W3215429829 hasConcept C126322002 @default.
• W3215429829 hasConcept C127561419 @default.
• W3215429829 hasConcept C134018914 @default.

• next