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dc.contributor.author이수영*
dc.contributor.author신동해*
dc.contributor.author심현보*
dc.contributor.author김완규*
dc.contributor.author김수원*
dc.contributor.author김지희*
dc.date.accessioned2024-05-20T16:31:18Z-
dc.date.available2024-05-20T16:31:18Z-
dc.date.issued2024*
dc.identifier.issn2041-1723*
dc.identifier.otherOAK-34854*
dc.identifier.urihttps://dspace.ewha.ac.kr/handle/2015.oak/268480-
dc.description.abstractOsteoarthritis (OA) is a progressive and irreversible degenerative joint disease that is characterized by cartilage destruction, osteophyte formation, subchondral bone remodeling, and synovitis. Despite affecting millions of patients, effective and safe disease-modifying osteoarthritis drugs are lacking. Here we reveal an unexpected role for the small molecule 5-aminosalicylic acid (5-ASA), which is used as an anti-inflammatory drug in ulcerative colitis. We show that 5-ASA competes with extracellular-matrix collagen-II to bind to osteoclast-associated receptor (OSCAR) on chondrocytes. Intra-articular 5-ASA injections ameliorate OA generated by surgery-induced medial-meniscus destabilization in male mice. Significantly, this effect is also observed when 5-ASA was administered well after OA onset. Moreover, mice with DMM-induced OA that are treated with 5-ASA at weeks 8–11 and sacrificed at week 12 have thicker cartilage than untreated mice that were sacrificed at week 8. Mechanistically, 5-ASA reverses OSCAR-mediated transcriptional repression of PPARγ in articular chondrocytes, thereby suppressing COX-2-related inflammation. It also improves chondrogenesis, strongly downregulates ECM catabolism, and promotes ECM anabolism. Our results suggest that 5-ASA could serve as a DMOAD. © The Author(s) 2024.*
dc.languageEnglish*
dc.publisherNature Research*
dc.title5-aminosalicylic acid suppresses osteoarthritis through the OSCAR-PPARγ axis*
dc.typeArticle*
dc.relation.issue1*
dc.relation.volume15*
dc.relation.indexSCIE*
dc.relation.indexSCOPUS*
dc.relation.journaltitleNature Communications*
dc.identifier.doi10.1038/s41467-024-45174-6*
dc.identifier.wosidWOS:001156769400015*
dc.identifier.scopusid2-s2.0-85184100287*
dc.author.googleKim*
dc.author.googleJihee*
dc.author.googleRyu*
dc.author.googleGina*
dc.author.googleSeo*
dc.author.googleJeongmin*
dc.author.googleGo*
dc.author.googleMiyeon*
dc.author.googleGyungmin*
dc.author.googleYi*
dc.author.googleSol*
dc.author.googleSuwon*
dc.author.googleLee*
dc.author.googleHana*
dc.author.googleJune-Yong*
dc.author.googleHan Sung*
dc.author.googlePark*
dc.author.googleMin-Chan*
dc.author.googleShin*
dc.author.googleDong Hae*
dc.author.googleShim*
dc.author.googleHyunbo*
dc.author.googleWankyu*
dc.author.googleSoo Young*
dc.contributor.scopusid이수영(53980218900;7409697278)*
dc.contributor.scopusid신동해(57217374185)*
dc.contributor.scopusid심현보(26635827900)*
dc.contributor.scopusid김완규(25627654100)*
dc.contributor.scopusid김수원(57193241841)*
dc.contributor.scopusid김지희(57210213807)*
dc.date.modifydate20240601081000*
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자연과학대학 > 생명과학전공 > Journal papers
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