{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1361699994648526080.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1111/j.1749-6632.2011.06258.x"}},{"identifier":{"@type":"URI","@value":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.1749-6632.2011.06258.x"}},{"identifier":{"@type":"URI","@value":"https://nyaspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1749-6632.2011.06258.x"}}],"dc:title":[{"@value":"Recent progress in understanding molecular mechanisms of cartilage degeneration during osteoarthritis"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p><jats:bold>Osteoarthritis (OA) is a highly prevalent disease affecting more than 20% of American adults. Predispositions include joint injury, heredity, obesity, and aging. Biomechanical alterations are commonly involved. However, the molecular mechanisms of this disease are complex, and there is currently no effective disease‐modifying treatment. The initiation and progression of OA subtypes is a complex process that at the molecular level probably involves many cell types, signaling pathways, and changes in extracellular matrix. <jats:italic>Ex vivo</jats:italic> studies with tissue derived from OA patients and <jats:italic>in vivo</jats:italic> studies with mutant mice have suggested that pathways involving receptor ligands such as TGF‐β1, WNT3a, and Indian hedgehog; signaling molecules such as Smads, β‐catenin, and HIF‐2a; and peptidases such as MMP13 and ADAMTS4/5 are probably involved to some degree. This review focuses on molecular mechanisms of OA development related to recent findings.</jats:bold></jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1381699994648526082","@type":"Researcher","foaf:name":[{"@value":"Meina Wang"}]},{"@id":"https://cir.nii.ac.jp/crid/1381699994648526083","@type":"Researcher","foaf:name":[{"@value":"Jie Shen"}]},{"@id":"https://cir.nii.ac.jp/crid/1381699994648526084","@type":"Researcher","foaf:name":[{"@value":"Hongting Jin"}]},{"@id":"https://cir.nii.ac.jp/crid/1380298340613949440","@type":"Researcher","foaf:name":[{"@value":"Hee‐Jeong Im"}]},{"@id":"https://cir.nii.ac.jp/crid/1381699994648526085","@type":"Researcher","foaf:name":[{"@value":"John Sandy"}]},{"@id":"https://cir.nii.ac.jp/crid/1381699994648526080","@type":"Researcher","foaf:name":[{"@value":"Di Chen"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00778923"},{"@type":"EISSN","@value":"17496632"}],"prism:publicationName":[{"@value":"Annals of the New York Academy of Sciences"}],"dc:publisher":[{"@value":"Wiley"}],"prism:publicationDate":"2011-12","prism:volume":"1240","prism:number":"1","prism:startingPage":"61","prism:endingPage":"69"},"reviewed":"false","dc:rights":["http://onlinelibrary.wiley.com/termsAndConditions#vor"],"url":[{"@id":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.1749-6632.2011.06258.x"},{"@id":"https://nyaspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1749-6632.2011.06258.x"}],"createdAt":"2011-12-15","modifiedAt":"2023-09-25","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360002216828055040","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Deletion of Runx2 in Articular Chondrocytes Decelerates the Progression of DMM-Induced Osteoarthritis in Adult Mice"}]},{"@id":"https://cir.nii.ac.jp/crid/1360004230249024384","@type":"Article","resourceType":"学術雑誌論文(journal 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