@prefix ocrer: <http://purl.org/net/OCRe/research.owl#> .
@prefix owl:   <http://www.w3.org/2002/07/owl#> .
@prefix scires: <http://vivoweb.org/ontology/scientific-research#> .
@prefix xsd:   <http://www.w3.org/2001/XMLSchema#> .
@prefix skos:  <http://www.w3.org/2004/02/skos/core#> .
@prefix rdfs:  <http://www.w3.org/2000/01/rdf-schema#> .
@prefix ocresd: <http://purl.org/net/OCRe/study_design.owl#> .
@prefix swo:   <http://www.ebi.ac.uk/efo/swo/> .
@prefix cito:  <http://purl.org/spar/cito/> .
@prefix geo:   <http://aims.fao.org/aos/geopolitical.owl#> .
@prefix ocresst: <http://purl.org/net/OCRe/statistics.owl#> .
@prefix dcterms: <http://purl.org/dc/terms/> .
@prefix vivo:  <http://vivoweb.org/ontology/core#> .
@prefix event: <http://purl.org/NET/c4dm/event.owl#> .
@prefix vann:  <http://purl.org/vocab/vann/> .
@prefix foaf:  <http://xmlns.com/foaf/0.1/> .
@prefix c4o:   <http://purl.org/spar/c4o/> .
@prefix fabio: <http://purl.org/spar/fabio/> .
@prefix vcard: <http://www.w3.org/2006/vcard/ns#> .
@prefix thkoeln: <http://cris.nrw/hisinone#> .
@prefix vitro: <http://vitro.mannlib.cornell.edu/ns/vitro/0.7#> .
@prefix vitro-public: <http://vitro.mannlib.cornell.edu/ns/vitro/public#> .
@prefix rdf:   <http://www.w3.org/1999/02/22-rdf-syntax-ns#> .
@prefix ocresp: <http://purl.org/net/OCRe/study_protocol.owl#> .
@prefix bibo:  <http://purl.org/ontology/bibo/> .
@prefix obo:   <http://purl.obolibrary.org/obo/> .
@prefix ro:    <http://purl.obolibrary.org/obo/ro.owl#> .

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        rdfs:label                "Naunyn-Schmiedebergs Archiv für Pharmakologie" ;
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        a             obo:BFO_0000001 , obo:BFO_0000020 , vivo:Authorship , vivo:Relationship , obo:BFO_0000002 , owl:Thing ;
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        a                         obo:IAO_0000030 , thkoeln:Publikation , foaf:Document , obo:BFO_0000001 , bibo:Document , owl:Thing , thkoeln:Journalartikel , obo:BFO_0000002 , obo:BFO_0000031 , thkoeln:Artikel ;
        rdfs:label                "Protective Effects of Gαi₃ Deficiency in a Murine Heart-Failure Model of β₁-Adrenoceptor Overexpression" , "RDF description of Protective Effects of Gαi₃ Deficiency in a Murine Heart-Failure Model of β₁-Adrenoceptor Overexpression - https://fis.th-koeln.de/vivo/individual/publ_13399" ;
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        thkoeln:sprache           "englisch" ;
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                <https://fis.th-koeln.de/vivo/individual/FF_001> ;
        <http://cris.nrw/hisinone/hatOrganisationseinheit>
                <https://fis.th-koeln.de/vivo/individual/eigene_HS> , <https://fis.th-koeln.de/vivo/individual/10000159> ;
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                <http://cris.nrw/hisinone/RessourceText> ;
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                <https://fis.th-koeln.de/vivo/individual/cite_13399-1> , <https://fis.th-koeln.de/vivo/individual/cite_13399-0> , <https://fis.th-koeln.de/vivo/individual/cite_13399-2> ;
        <http://cris.nrw/hisinone/hatZugangsrecht>
                <http://cris.nrw/hisinone/OpenAccess> ;
        <http://purl.org/dc/elements/1.1/date>
                "2026-04-04T06:21:43"^^xsd:dateTime ;
        <http://purl.org/dc/elements/1.1/publisher>
                <https://fis.th-koeln.de/vivo> ;
        <http://purl.org/dc/elements/1.1/rights>
                <https://fis.th-koeln.de/vivo/termsOfUse> ;
        bibo:abstract             "We have shown that in murine cardiomyopathy caused by overexpression of the β₁-adrenoceptor, Gαi₂-deficiency is detrimental. Given the growing evidence for isoform-specific Gαi-functions, we now examined the consequences of Gαi₃ deficiency in the same heart-failure model. Mice overexpressing cardiac β₁-adrenoceptors with (β₁-tg) or without Gαi₃-expression (β₁-tg/Gαi₃−/−) were compared to C57BL/6 wildtypes and global Gαi₃-knockouts (Gαi₃−/−). The life span of β₁-tg mice was significantly shortened but improved when Gαi₃ was lacking (95% CI: 592–655 vs. 644–747 days). At 300 days of age, left-ventricular function and survival rate were similar in all groups. At 550 days of age, β₁-tg but not β₁-tg/Gαi₃−/− mice displayed impaired ejection fraction (35 ± 18% vs. 52 ± 16%) compared to wildtype (59 ± 4%) and Gαi₃−/− mice (60 ± 5%). Diastolic dysfunction of β₁-tg mice was prevented by Gαi₃ deficiency, too. The increase of ANP mRNA levels and ventricular fibrosis observed in β₁-tg hearts was significantly attenuated in β₁-tg/Gαi₃−/− mice. Transcript levels of phospholamban, ryanodine receptor 2, and cardiac troponin I were similar in all groups. However, Western blots and phospho-proteomic analyses showed that in β₁-tg, but not β₁-tg/Gαi₃−/− ventricles, phospholamban protein was reduced while its phosphorylation increased. Here, we show that in mice overexpressing the cardiac β₁-adrenoceptor, Gαi₃ deficiency slows or even prevents cardiomyopathy and increases shortened life span. Previously, we found Gαi₂ deficiency to aggravate cardiac dysfunction and mortality in the same heart-failure model. Our findings indicate isoform-specific interventions into Gi-dependent signaling to be promising cardio-protective strategies." ;
        bibo:doi                  "10.1007/s00210-023-02751-8" ;
        vitro:mostSpecificType    thkoeln:Journalartikel ;
        vivo:dateTimeValue        <http://cris.nrw/date2023> ;
        vivo:freetextKeyword      "Gi Protein" , "Cardiomyopathy" , "Adrenergic Receptor" , "Heart Failure" , "Cardioprotection" ;
        vivo:hasPublicationVenue  <https://fis.th-koeln.de/vivo/individual/journal_1528> ;
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