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http://purl.uniprot.org/citations/34987154http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/34987154http://www.w3.org/2000/01/rdf-schema#comment"Here, in Ppara-/- mice, we found that an increased DNL stimulated the cartilage degradation and identified ACOT12 as a key regulatory factor. Suppressed level of ACOT12 was observed in cartilages of OA patient and OA-induced animal. To determine the role and association of ACOT12 in the OA pathogenesis, we generated Acot12 knockout (KO) (Acot12-/-) mice using RNA-guided endonuclease. Acot12-/- mice displayed the severe cartilage degradation with the stimulation of matrix MMPs and chondrocyte apoptosis through the accumulation of acetyl CoA. Delivery of acetyl CoA-conjugated chitosan complex into cartilage stimulated DNL and cartilage degradation. Moreover, restoration of ACOT12 into human OA chondrocytes and OA-induced mouse cartilage effectively rescued the pathophysiological features of OA by regulating DNL. Taken together, our study suggested ACOT12 as a novel regulatory factor in maintaining cartilage homeostasis and targeting ACOT12 could contribute to developing a new therapeutic strategy for OA."xsd:string
http://purl.uniprot.org/citations/34987154http://purl.org/dc/terms/identifier"doi:10.1038/s41467-021-27738-y"xsd:string
http://purl.uniprot.org/citations/34987154http://purl.uniprot.org/core/author"Park S."xsd:string
http://purl.uniprot.org/citations/34987154http://purl.uniprot.org/core/author"Ryu J.H."xsd:string
http://purl.uniprot.org/citations/34987154http://purl.uniprot.org/core/author"Baek I.J."xsd:string
http://purl.uniprot.org/citations/34987154http://purl.uniprot.org/core/author"Chun C.H."xsd:string
http://purl.uniprot.org/citations/34987154http://purl.uniprot.org/core/author"Jin E.J."xsd:string
http://purl.uniprot.org/citations/34987154http://purl.uniprot.org/core/date"2022"xsd:gYear
http://purl.uniprot.org/citations/34987154http://purl.uniprot.org/core/name"Nat Commun"xsd:string
http://purl.uniprot.org/citations/34987154http://purl.uniprot.org/core/pages"3"xsd:string
http://purl.uniprot.org/citations/34987154http://purl.uniprot.org/core/title"PPARalpha-ACOT12 axis is responsible for maintaining cartilage homeostasis through modulating de novo lipogenesis."xsd:string
http://purl.uniprot.org/citations/34987154http://purl.uniprot.org/core/volume"13"xsd:string
http://purl.uniprot.org/citations/34987154http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/34987154
http://purl.uniprot.org/citations/34987154http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/34987154
http://purl.uniprot.org/uniprot/#_A2RSC2-mappedCitation-34987154http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34987154
http://purl.uniprot.org/uniprot/#_Q9DBK0-mappedCitation-34987154http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34987154
http://purl.uniprot.org/uniprot/A2RSC2http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/34987154
http://purl.uniprot.org/uniprot/Q9DBK0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/34987154