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http://purl.uniprot.org/citations/26224885http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26224885http://www.w3.org/2000/01/rdf-schema#comment"Obesity is increasing in prevalence and is strongly associated with metabolic and cardiovascular disorders. The renin-angiotensin system (RAS) has emerged as a key pathogenic mechanism for these disorders; angiotensin (Ang)-converting enzyme 2 (ACE2) negatively regulates RAS by metabolizing Ang II into Ang 1-7. We studied the role of ACE2 in obesity-mediated cardiac dysfunction. ACE2 null (ACE2KO) and wild-type (WT) mice were fed a high-fat diet (HFD) or a control diet and studied at 6 months of age. Loss of ACE2 resulted in decreased weight gain but increased glucose intolerance, epicardial adipose tissue (EAT) inflammation, and polarization of macrophages into a proinflammatory phenotype in response to HFD. Similarly, human EAT in patients with obesity and heart failure displayed a proinflammatory macrophage phenotype. Exacerbated EAT inflammation in ACE2KO-HFD mice was associated with decreased myocardial adiponectin, decreased phosphorylation of AMPK, increased cardiac steatosis and lipotoxicity, and myocardial insulin resistance, which worsened heart function. Ang 1-7 (24 µg/kg/h) administered to ACE2KO-HFD mice resulted in ameliorated EAT inflammation and reduced cardiac steatosis and lipotoxicity, resulting in normalization of heart failure. In conclusion, ACE2 plays a novel role in heart disease associated with obesity wherein ACE2 negatively regulates obesity-induced EAT inflammation and cardiac insulin resistance."xsd:string
http://purl.uniprot.org/citations/26224885http://purl.org/dc/terms/identifier"doi:10.2337/db15-0399"xsd:string
http://purl.uniprot.org/citations/26224885http://purl.uniprot.org/core/author"Mori J."xsd:string
http://purl.uniprot.org/citations/26224885http://purl.uniprot.org/core/author"Patel V.B."xsd:string
http://purl.uniprot.org/citations/26224885http://purl.uniprot.org/core/author"Basu R."xsd:string
http://purl.uniprot.org/citations/26224885http://purl.uniprot.org/core/author"Das S.K."xsd:string
http://purl.uniprot.org/citations/26224885http://purl.uniprot.org/core/author"Oudit G.Y."xsd:string
http://purl.uniprot.org/citations/26224885http://purl.uniprot.org/core/author"Penninger J.M."xsd:string
http://purl.uniprot.org/citations/26224885http://purl.uniprot.org/core/author"Parajuli N."xsd:string
http://purl.uniprot.org/citations/26224885http://purl.uniprot.org/core/author"Lopaschuk G.D."xsd:string
http://purl.uniprot.org/citations/26224885http://purl.uniprot.org/core/author"Grant M.B."xsd:string
http://purl.uniprot.org/citations/26224885http://purl.uniprot.org/core/author"Ramprasath T."xsd:string
http://purl.uniprot.org/citations/26224885http://purl.uniprot.org/core/author"McLean B.A."xsd:string
http://purl.uniprot.org/citations/26224885http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/26224885http://purl.uniprot.org/core/name"Diabetes"xsd:string
http://purl.uniprot.org/citations/26224885http://purl.uniprot.org/core/pages"85-95"xsd:string
http://purl.uniprot.org/citations/26224885http://purl.uniprot.org/core/title"ACE2 Deficiency Worsens Epicardial Adipose Tissue Inflammation and Cardiac Dysfunction in Response to Diet-Induced Obesity."xsd:string
http://purl.uniprot.org/citations/26224885http://purl.uniprot.org/core/volume"65"xsd:string
http://purl.uniprot.org/citations/26224885http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/26224885
http://purl.uniprot.org/citations/26224885http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/26224885
http://purl.uniprot.org/uniprot/#_C7ECU2-mappedCitation-26224885http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26224885
http://purl.uniprot.org/uniprot/#_F6X479-mappedCitation-26224885http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26224885
http://purl.uniprot.org/uniprot/#_Q3UXR1-mappedCitation-26224885http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26224885
http://purl.uniprot.org/uniprot/#_Q3URC9-mappedCitation-26224885http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26224885