| pubmed-article:19823586 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19823586 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
| pubmed-article:19823586 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:19823586 | lifeskim:mentions | umls-concept:C0031437 | lld:lifeskim |
| pubmed-article:19823586 | lifeskim:mentions | umls-concept:C1555029 | lld:lifeskim |
| pubmed-article:19823586 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:19823586 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:19823586 | pubmed:dateCreated | 2009-10-13 | lld:pubmed |
| pubmed-article:19823586 | pubmed:abstractText | Fibrosis, the excessive deposition of scar tissue by fibroblasts, is one of the largest groups of diseases for which there is no therapy. Fibroblasts from lesional areas of scleroderma patients possess elevated abilities to contract matrix and produce alpha-smooth muscle actin (alpha-SMA), type I collagen and CCN2 (connective tissue growth factor, CTGF). The basis for this phenomenon is poorly understood, and is a necessary prerequisite for developing novel, rational anti-fibrotic strategies. | lld:pubmed |
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| pubmed-article:19823586 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:19823586 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19823586 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19823586 | pubmed:issn | 1932-6203 | lld:pubmed |
| pubmed-article:19823586 | pubmed:author | pubmed-author:LeaskAndrewA | lld:pubmed |
| pubmed-article:19823586 | pubmed:author | pubmed-author:AbrahamDavid... | lld:pubmed |
| pubmed-article:19823586 | pubmed:author | pubmed-author:EastwoodMarkM | lld:pubmed |
| pubmed-article:19823586 | pubmed:author | pubmed-author:DentonChristo... | lld:pubmed |
| pubmed-article:19823586 | pubmed:author | pubmed-author:Shi-wenXuX | lld:pubmed |
| pubmed-article:19823586 | pubmed:author | pubmed-author:LiuShangxiS | lld:pubmed |
| pubmed-article:19823586 | pubmed:author | pubmed-author:SonnylalSonal... | lld:pubmed |
| pubmed-article:19823586 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19823586 | pubmed:volume | 4 | lld:pubmed |
| pubmed-article:19823586 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19823586 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19823586 | pubmed:pagination | e7438 | lld:pubmed |
| pubmed-article:19823586 | pubmed:dateRevised | 2010-9-28 | lld:pubmed |
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| pubmed-article:19823586 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19823586 | pubmed:articleTitle | Rac inhibition reverses the phenotype of fibrotic fibroblasts. | lld:pubmed |
| pubmed-article:19823586 | pubmed:affiliation | Centre for Rheumatology, Department of Medicine, University College London (Royal Free Campus), London, United Kingdom. | lld:pubmed |
| pubmed-article:19823586 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19823586 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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