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http://purl.uniprot.org/citations/28465484http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28465484http://www.w3.org/2000/01/rdf-schema#comment"Renal fibrosis participates in the progression of hypertension-induced kidney injury. The effect of SIRT3, a member of the NAD+-dependent deacetylase family, in hypertensive nephropathy remains unclear. In this study, we found that SIRT3 was reduced after angiotensin II (AngII) treatment both in vivo and in vitro. Furthermore, SIRT3-knockout mice aggravated hypertension-induced renal dysfunction and renal fibrosis via chronic AngII infusion (2000 ng/kg per minute for 42 days). On the contrary, SIRT3-overexpression mice attenuated AngII-induced kidney injury compared with wild-type mice. Remarkably, a co-localization of SIRT3 and KLF15, a kidney-enriched nuclear transcription factor, led to SIRT3 directly deacetylating KLF15, followed by decreased expression of fibronectin and collagen type IV in cultured MPC-5 podocytes. In addition, honokiol (HKL), a major bioactive compound isolated from Magnolia officinalis (Houpo), suppressed AngII-induced renal fibrosis through activating SIRT3-KLF15 signaling. Taken together, our findings implicate that a novel SIRT3-KLF15 signaling may prevent kidney injury from hypertension and HKL can act as a SIRT3-KLF15 signaling activator to protect against hypertensive nephropathy."xsd:string
http://purl.uniprot.org/citations/28465484http://purl.org/dc/terms/identifier"doi:10.18632/oncotarget.17165"xsd:string
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/author"Liu H."xsd:string
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/author"Li N."xsd:string
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/author"Huang C."xsd:string
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/author"Zhang Y."xsd:string
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/author"Zhang P."xsd:string
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/author"Zhang J."xsd:string
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/author"Zhang C."xsd:string
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/author"Yan X."xsd:string
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/author"Yang Y."xsd:string
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/author"Shan X."xsd:string
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/author"Bu P."xsd:string
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/name"Oncotarget"xsd:string
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/pages"39592-39604"xsd:string
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/title"SIRT3-KLF15 signaling ameliorates kidney injury induced by hypertension."xsd:string
http://purl.uniprot.org/citations/28465484http://purl.uniprot.org/core/volume"8"xsd:string
http://purl.uniprot.org/citations/28465484http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/28465484
http://purl.uniprot.org/citations/28465484http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/28465484
http://purl.uniprot.org/uniprot/#_A0A0N4SVC6-mappedCitation-28465484http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28465484
http://purl.uniprot.org/uniprot/#_D3YVQ5-mappedCitation-28465484http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28465484
http://purl.uniprot.org/uniprot/#_D3YWD6-mappedCitation-28465484http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28465484