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Osteoclast-associated receptor blockade prevents articular cartilage destruction via chondrocyte apoptosis regulation

DC FieldValueLanguage
dc.contributor.author박민찬-
dc.date.accessioned2020-09-30T16:46:37Z-
dc.date.available2020-09-30T16:46:37Z-
dc.date.issued2020-08-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/179619-
dc.description.abstractOsteoarthritis (OA), primarily characterized by articular cartilage destruction, is the most common form of age-related degenerative whole-joint disease. No disease-modifying treatments for OA are currently available. Although OA is primarily characterized by cartilage destruction, our understanding of the processes controlling OA progression is poor. Here, we report the association of OA with increased levels of osteoclast-associated receptor (OSCAR), an immunoglobulin-like collagen-recognition receptor. In mice, OSCAR deletion abrogates OA manifestations, such as articular cartilage destruction, subchondral bone sclerosis, and hyaline cartilage loss. These effects are a result of decreased chondrocyte apoptosis, which is caused by the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in induced OA. Treatments with human OSCAR-Fc fusion protein attenuates OA pathogenesis caused by experimental OA. Thus, this work highlights the function of OSCAR as a catabolic regulator of OA pathogenesis, indicating that OSCAR blockade is a potential therapy for OA.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherNature Pub. Group-
dc.relation.isPartOfNATURE COMMUNICATIONS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleOsteoclast-associated receptor blockade prevents articular cartilage destruction via chondrocyte apoptosis regulation-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학교실)-
dc.contributor.googleauthorDoo Ri Park-
dc.contributor.googleauthorJihee Kim-
dc.contributor.googleauthorGyeong Min Kim-
dc.contributor.googleauthorHaeseung Lee-
dc.contributor.googleauthorMinhee Kim-
dc.contributor.googleauthorDonghyun Hwang-
dc.contributor.googleauthorHana Lee-
dc.contributor.googleauthorHan-Sung Kim-
dc.contributor.googleauthorWankyu Kim-
dc.contributor.googleauthorMin Chan Park-
dc.contributor.googleauthorHyunbo Shim-
dc.contributor.googleauthorSoo Young Lee-
dc.identifier.doi10.1038/s41467-020-18208-y-
dc.contributor.localIdA01470-
dc.relation.journalcodeJ02293-
dc.identifier.eissn2041-1723-
dc.identifier.pmid32859940-
dc.contributor.alternativeNamePark, Min Chan-
dc.contributor.affiliatedAuthor박민찬-
dc.citation.volume11-
dc.citation.number1-
dc.citation.startPage4343-
dc.identifier.bibliographicCitationNATURE COMMUNICATIONS, Vol.11(1) : 4343, 2020-08-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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