| pubmed-article:9591765 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9591765 | lifeskim:mentions | umls-concept:C0030705 | lld:lifeskim |
| pubmed-article:9591765 | lifeskim:mentions | umls-concept:C0027061 | lld:lifeskim |
| pubmed-article:9591765 | lifeskim:mentions | umls-concept:C0007193 | lld:lifeskim |
| pubmed-article:9591765 | lifeskim:mentions | umls-concept:C0623362 | lld:lifeskim |
| pubmed-article:9591765 | lifeskim:mentions | umls-concept:C0041904 | lld:lifeskim |
| pubmed-article:9591765 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
| pubmed-article:9591765 | lifeskim:mentions | umls-concept:C1150224 | lld:lifeskim |
| pubmed-article:9591765 | lifeskim:mentions | umls-concept:C0205088 | lld:lifeskim |
| pubmed-article:9591765 | pubmed:issue | 17 | lld:pubmed |
| pubmed-article:9591765 | pubmed:dateCreated | 1998-5-28 | lld:pubmed |
| pubmed-article:9591765 | pubmed:abstractText | One of the hallmarks of dilated cardiomyopathy (DCM) is left ventricular (LV) remodeling. The matrix metalloproteinases (MMPs) are a family of enzymes that contribute to extracellular remodeling in several disease states. Additionally, a family of inhibitors called tissue inhibitors of MMPs (TIMPs) has been shown to exist and to tightly regulate MMP activity. However, the types of MMPs and TIMPs expressed within the normal and DCM LV myocardium and the relation to MMP activity remain unexplored. | lld:pubmed |
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| pubmed-article:9591765 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9591765 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:9591765 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9591765 | pubmed:month | May | lld:pubmed |
| pubmed-article:9591765 | pubmed:issn | 0009-7322 | lld:pubmed |
| pubmed-article:9591765 | pubmed:author | pubmed-author:SpinaleF GFG | lld:pubmed |
| pubmed-article:9591765 | pubmed:author | pubmed-author:CrumbleyA... | lld:pubmed |
| pubmed-article:9591765 | pubmed:author | pubmed-author:ZellnerJ LJL | lld:pubmed |
| pubmed-article:9591765 | pubmed:author | pubmed-author:ThomasC VCV | lld:pubmed |
| pubmed-article:9591765 | pubmed:author | pubmed-author:HandyJ RJR | lld:pubmed |
| pubmed-article:9591765 | pubmed:author | pubmed-author:CokerM LML | lld:pubmed |
| pubmed-article:9591765 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9591765 | pubmed:day | 5 | lld:pubmed |
| pubmed-article:9591765 | pubmed:volume | 97 | lld:pubmed |
| pubmed-article:9591765 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9591765 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9591765 | pubmed:pagination | 1708-15 | lld:pubmed |
| pubmed-article:9591765 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:9591765 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9591765 | pubmed:articleTitle | Increased matrix metalloproteinase activity and selective upregulation in LV myocardium from patients with end-stage dilated cardiomyopathy. | lld:pubmed |
| pubmed-article:9591765 | pubmed:affiliation | Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston 29425, USA. | lld:pubmed |
| pubmed-article:9591765 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9591765 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9591765 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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