FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2972167790> ?p ?o ?g. }

• W2972167790 abstract "ABSTRACT Background Eosinophil count predicts outcome following myocardial infarction (MI) and eosinophils regulate tissue repair and regeneration in extra-cardiac settings. Objectives To investigate the role of eosinophils in regulating inflammation, repair and remodelling following MI. Methods Blood eosinophil count was assessed in 732 patients undergoing primary percutaneous coronary intervention for ST-segment elevation MI (STEMI). Experimental MI was induced in wild-type (WT) and eosinophil-depleted mice (ΔdblGATA or anti-Siglec F antibody treated). Cardiac function was characterised by high-resolution ultrasound and immune cell infiltration by flow cytometry of infarct digests. Results Blood eosinophil count declined in the hours following STEMI in patients and following MI induction in mice. Eosinophils were subsequently identified in the myocardium of patients and mice. Genetic eosinophil depletion in mice increased LV dilatation (end-systolic area: 29.0±2.2cm 2 v 21.6±1.6cm 2 ; p=0.02) and reduced ejection fraction (22.0±3.6% v 34.3±4.0% in p=0.04,) in ΔdblGATA v WT following MI (n=8-9/group), an outcome reproduced by pharmacological depletion. ΔdblGATA mice had increased scar size with disrupted collagen deposition and altered expression of the collagen cross-linking genes plod2 and lox . CD206 + pro-repair macrophages were less prevalent in the infarct zone of ΔdblGATA mice (27.0±2.3% v WT: 39.2.4±3.5%; p=0.01, n=9-11/group) but were restored by replenishment with bone marrow-derived eosinophils. Anti-inflammatory cytokine concentrations were reduced in ΔdblGATA mice and IL-4 complex administration 24h after MI rescued adverse remodelling. Conclusions Eosinophils are recruited to the heart following MI and are required for effective repair and to prevent adverse remodelling. IL-4 therapy has potential to limit detrimental outcomes when eosinophil availability is low. HIGHLIGHTS A drop in eosinophil blood count is associated with recruitment of eosinophils to the heart during repair following clinical and experimental myocardial infarction. Genetic & pharmacological eosinophil depletion leads to increased adverse remodelling in experimental MI. Eosinophils are required for aquisition of an anti-inflammatory macrophage phenotype and a shift to resolution of inflammation during infarct repair. Interleukin-4 therapy is able to rescue the adverse remodelling phenotype in conditions of eosinophil deficiency. Condensed abstract In ST-segment elevation myocardial infarction (STEMI) of both patients and mice, there was a decline in blood eosinophil count, with activated eosinophils recruited to the infarct zone. Eosinophil deficiency resulted in attenuated anti-inflammatory pro-repair macrophage polarization, enhanced myocardial inflammation, increased scar size and deterioration of myocardial structure and function. Adverse cardiac remodelling in the setting of eosinophil deficiency was prevented by IL-4 therapy." @default.
• W2972167790 created "2019-09-12" @default.
• W2972167790 creator A5016074421 @default.
• W2972167790 creator A5016151265 @default.
• W2972167790 creator A5020545657 @default.
• W2972167790 creator A5023563270 @default.
• W2972167790 creator A5023653821 @default.
• W2972167790 creator A5027867579 @default.
• W2972167790 creator A5028598758 @default.
• W2972167790 creator A5035492513 @default.
• W2972167790 creator A5036916652 @default.
• W2972167790 creator A5037137972 @default.
• W2972167790 creator A5059874316 @default.
• W2972167790 creator A5065112664 @default.
• W2972167790 creator A5074252129 @default.
• W2972167790 creator A5076588854 @default.
• W2972167790 creator A5077994275 @default.
• W2972167790 creator A5080125880 @default.
• W2972167790 date "2019-09-09" @default.
• W2972167790 modified "2023-10-16" @default.
• W2972167790 title "Eosinophil deficiency promotes aberrant repair and adverse remodelling following acute myocardial infarction" @default.
• W2972167790 cites W1513224400 @default.
• W2972167790 cites W1691245493 @default.
• W2972167790 cites W1761798697 @default.
• W2972167790 cites W1981083100 @default.
• W2972167790 cites W1982925783 @default.
• W2972167790 cites W1999353686 @default.
• W2972167790 cites W2009122936 @default.
• W2972167790 cites W2018473648 @default.
• W2972167790 cites W2033946555 @default.
• W2972167790 cites W2065833808 @default.
• W2972167790 cites W2069406253 @default.
• W2972167790 cites W2077783398 @default.
• W2972167790 cites W2125951365 @default.
• W2972167790 cites W2135647797 @default.
• W2972167790 cites W2142760199 @default.
• W2972167790 cites W2145655023 @default.
• W2972167790 cites W2156056478 @default.
• W2972167790 cites W2157758580 @default.
• W2972167790 cites W2345479752 @default.
• W2972167790 cites W2519720623 @default.
• W2972167790 cites W2550245417 @default.
• W2972167790 cites W2559504276 @default.
• W2972167790 cites W2616059982 @default.
• W2972167790 cites W2727904536 @default.
• W2972167790 cites W2739074538 @default.
• W2972167790 cites W4293577771 @default.
• W2972167790 doi "https://doi.org/10.1101/750133" @default.
• W2972167790 hasPublicationYear "2019" @default.
• W2972167790 type Work @default.
• W2972167790 sameAs 2972167790 @default.
• W2972167790 citedByCount "2" @default.
• W2972167790 countsByYear W29721677902020 @default.
• W2972167790 countsByYear W29721677902022 @default.
• W2972167790 crossrefType "posted-content" @default.
• W2972167790 hasAuthorship W2972167790A5016074421 @default.
• W2972167790 hasAuthorship W2972167790A5016151265 @default.
• W2972167790 hasAuthorship W2972167790A5020545657 @default.
• W2972167790 hasAuthorship W2972167790A5023563270 @default.
• W2972167790 hasAuthorship W2972167790A5023653821 @default.
• W2972167790 hasAuthorship W2972167790A5027867579 @default.
• W2972167790 hasAuthorship W2972167790A5028598758 @default.
• W2972167790 hasAuthorship W2972167790A5035492513 @default.
• W2972167790 hasAuthorship W2972167790A5036916652 @default.
• W2972167790 hasAuthorship W2972167790A5037137972 @default.
• W2972167790 hasAuthorship W2972167790A5059874316 @default.
• W2972167790 hasAuthorship W2972167790A5065112664 @default.
• W2972167790 hasAuthorship W2972167790A5074252129 @default.
• W2972167790 hasAuthorship W2972167790A5076588854 @default.
• W2972167790 hasAuthorship W2972167790A5077994275 @default.
• W2972167790 hasAuthorship W2972167790A5080125880 @default.
• W2972167790 hasBestOaLocation W29721677901 @default.
• W2972167790 hasConcept C111566952 @default.
• W2972167790 hasConcept C121332964 @default.
• W2972167790 hasConcept C126322002 @default.
• W2972167790 hasConcept C153400128 @default.
• W2972167790 hasConcept C164705383 @default.
• W2972167790 hasConcept C203014093 @default.
• W2972167790 hasConcept C2776042228 @default.
• W2972167790 hasConcept C2776914184 @default.
• W2972167790 hasConcept C2777037409 @default.
• W2972167790 hasConcept C2778198053 @default.
• W2972167790 hasConcept C2780007613 @default.
• W2972167790 hasConcept C500558357 @default.
• W2972167790 hasConcept C71924100 @default.
• W2972167790 hasConcept C78085059 @default.
• W2972167790 hasConcept C97355855 @default.
• W2972167790 hasConceptScore W2972167790C111566952 @default.
• W2972167790 hasConceptScore W2972167790C121332964 @default.
• W2972167790 hasConceptScore W2972167790C126322002 @default.
• W2972167790 hasConceptScore W2972167790C153400128 @default.
• W2972167790 hasConceptScore W2972167790C164705383 @default.
• W2972167790 hasConceptScore W2972167790C203014093 @default.
• W2972167790 hasConceptScore W2972167790C2776042228 @default.
• W2972167790 hasConceptScore W2972167790C2776914184 @default.
• W2972167790 hasConceptScore W2972167790C2777037409 @default.
• W2972167790 hasConceptScore W2972167790C2778198053 @default.
• W2972167790 hasConceptScore W2972167790C2780007613 @default.
• W2972167790 hasConceptScore W2972167790C500558357 @default.
• W2972167790 hasConceptScore W2972167790C71924100 @default.

• next