Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 정익모 | * |
dc.date.accessioned | 2016-08-28T12:08:53Z | - |
dc.date.available | 2016-08-28T12:08:53Z | - |
dc.date.issued | 2008 | * |
dc.identifier.issn | 1011-8934 | * |
dc.identifier.other | OAK-4658 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/219967 | - |
dc.description.abstract | For the purpose of determining the pathogenic role of transforming growth factor-β1 (TGF-β1) in the mechanism of chronic rheumatic heart disease, we evaluated the expression of TGF-β1, proliferation of myofibroblasts, and changes in extracellular matrix components including collagen and proteoglycan in 30 rheumatic mitral valves and in 15 control valves. High TGF-β1 expression was identified in 21 cases (70%) of rheumatic mitral valves, whereas only 3 cases (20%) of the control group showed high TGF-β1 expression (p<0.001). Additionally, increased proliferation of myofibroblasts was observed in the rheumatic valves. High TGF-β1 expression positively correlated with the proliferation of myofibroblasts (p=0.004), valvular fibrosis (p< 0.001), inflammatory cell infiltration (p=0.004), neovascularization (p=0.007), and calcification (p<0.001) in the valvular leaflets. The ratio of proteoglycan to collagen deposition inversely correlated with TGF-β1 expression in mitral valves (p=0.040). In conclusion, an ongoing inflammatory process, the expression of TGF-β1, and proliferation of myofibroblasts within the valves have a potential role in the valvular fibrosis, calcification, and changes in the extracellular matrix that lead to the scarring sequelae of rheumatic heart disease. Copyright © The Korean Academy of Medical Sciences. | * |
dc.language | English | * |
dc.title | Overexpression of transforming growth factor-β1 in the valvular fibrosis of chronic rheumatic heart disease | * |
dc.type | Article | * |
dc.relation.issue | 1 | * |
dc.relation.volume | 23 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.index | KCI | * |
dc.relation.startpage | 41 | * |
dc.relation.lastpage | 48 | * |
dc.relation.journaltitle | Journal of Korean Medical Science | * |
dc.identifier.doi | 10.3346/jkms.2008.23.1.41 | * |
dc.identifier.wosid | WOS:000253823300007 | * |
dc.identifier.scopusid | 2-s2.0-40549085331 | * |
dc.author.google | Kim L. | * |
dc.author.google | Do K.K. | * |
dc.author.google | Woo I.Y. | * |
dc.author.google | Dong H.S. | * |
dc.author.google | Ick M.J. | * |
dc.author.google | Han K.P. | * |
dc.author.google | Byung C.C. | * |
dc.contributor.scopusid | 정익모(7201867918) | * |
dc.date.modifydate | 20231116123346 | * |