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http://purl.uniprot.org/citations/24170693http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24170693http://www.w3.org/2000/01/rdf-schema#comment"Chronic low-grade inflammation, particularly in the adipose tissue, orchestrates obesity-induced insulin resistance. In this process, polarized activation of macrophages plays a crucial role. However, how macrophages contribute to insulin resistance remains obscure. Class A scavenger receptor (SR-A) is a pattern recognition receptor primarily expressed in macrophages. Through a combination of in vivo and in vitro studies, we report here that deletion of SR-A resulted in reduced insulin sensitivity in obese mice. The anti-inflammatory virtue of SR-A was accomplished by favoring M2 macrophage polarization in adipose tissue. Moreover, we demonstrate that lysophosphatidylcholine (LPC) served as an obesity-related endogenous ligand for SR-A promoting M2 macrophage polarization by activation of signal transducer and activator of transcription 6 signaling. These data have unraveled a clear mechanistic link between insulin resistance and inflammation mediated by the LPC/SR-A pathway in macrophages."xsd:string
http://purl.uniprot.org/citations/24170693http://purl.org/dc/terms/identifier"doi:10.2337/db13-0815"xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/author"Chen Q."xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/author"Bai H."xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/author"Jiang Y."xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/author"Li X."xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/author"Ma K."xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/author"Zhang Y."xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/author"Yang Q."xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/author"Zhang H."xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/author"Zhu X."xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/author"Zhu L."xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/author"Xu Y."xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/author"Zong G."xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/author"Ben J."xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/name"Diabetes"xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/pages"562-577"xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/title"Deletion of class A scavenger receptor deteriorates obesity-induced insulin resistance in adipose tissue."xsd:string
http://purl.uniprot.org/citations/24170693http://purl.uniprot.org/core/volume"63"xsd:string
http://purl.uniprot.org/citations/24170693http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/24170693
http://purl.uniprot.org/citations/24170693http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/24170693
http://purl.uniprot.org/uniprot/#_A0A1B0GRS5-mappedCitation-24170693http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24170693
http://purl.uniprot.org/uniprot/#_Q3U2C3-mappedCitation-24170693http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24170693