| pubmed-article:9987071 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9987071 | lifeskim:mentions | umls-concept:C0017296 | lld:lifeskim |
| pubmed-article:9987071 | lifeskim:mentions | umls-concept:C0008109 | lld:lifeskim |
| pubmed-article:9987071 | lifeskim:mentions | umls-concept:C0017658 | lld:lifeskim |
| pubmed-article:9987071 | lifeskim:mentions | umls-concept:C0015350 | lld:lifeskim |
| pubmed-article:9987071 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
| pubmed-article:9987071 | lifeskim:mentions | umls-concept:C1517004 | lld:lifeskim |
| pubmed-article:9987071 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:9987071 | pubmed:dateCreated | 1999-4-15 | lld:pubmed |
| pubmed-article:9987071 | pubmed:abstractText | The evidence that transforming growth factor-beta (TGF-beta) is a key mediator in the pathogenesis of fibrotic diseases is now supported by several lines of investigation. This evidence provides a certain base for targeting TGF-beta as an antifibrotic agent. | lld:pubmed |
| pubmed-article:9987071 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9987071 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9987071 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9987071 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9987071 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9987071 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:9987071 | pubmed:issn | 0085-2538 | lld:pubmed |
| pubmed-article:9987071 | pubmed:author | pubmed-author:HoriMM | lld:pubmed |
| pubmed-article:9987071 | pubmed:author | pubmed-author:SudoTT | lld:pubmed |
| pubmed-article:9987071 | pubmed:author | pubmed-author:NAVAG CGC | lld:pubmed |
| pubmed-article:9987071 | pubmed:author | pubmed-author:BorderW AWA | lld:pubmed |
| pubmed-article:9987071 | pubmed:author | pubmed-author:AndoYY | lld:pubmed |
| pubmed-article:9987071 | pubmed:author | pubmed-author:ImaiEE | lld:pubmed |
| pubmed-article:9987071 | pubmed:author | pubmed-author:KanedaYY | lld:pubmed |
| pubmed-article:9987071 | pubmed:author | pubmed-author:NobleN ANA | lld:pubmed |
| pubmed-article:9987071 | pubmed:author | pubmed-author:AkagiYY | lld:pubmed |
| pubmed-article:9987071 | pubmed:author | pubmed-author:IsakaYY | lld:pubmed |
| pubmed-article:9987071 | pubmed:author | pubmed-author:TsujieMM | lld:pubmed |
| pubmed-article:9987071 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9987071 | pubmed:volume | 55 | lld:pubmed |
| pubmed-article:9987071 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9987071 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9987071 | pubmed:pagination | 465-75 | lld:pubmed |
| pubmed-article:9987071 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:9987071 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:9987071 | pubmed:articleTitle | Gene therapy by transforming growth factor-beta receptor-IgG Fc chimera suppressed extracellular matrix accumulation in experimental glomerulonephritis. | lld:pubmed |
| pubmed-article:9987071 | pubmed:affiliation | First Department of Medicine, Osaka University School of Medicine, Japan. | lld:pubmed |
| pubmed-article:9987071 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9987071 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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