| pubmed-article:16319143 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16319143 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:16319143 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
| pubmed-article:16319143 | lifeskim:mentions | umls-concept:C0032214 | lld:lifeskim |
| pubmed-article:16319143 | lifeskim:mentions | umls-concept:C0600138 | lld:lifeskim |
| pubmed-article:16319143 | lifeskim:mentions | umls-concept:C0333186 | lld:lifeskim |
| pubmed-article:16319143 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:16319143 | pubmed:issue | 14 | lld:pubmed |
| pubmed-article:16319143 | pubmed:dateCreated | 2005-12-1 | lld:pubmed |
| pubmed-article:16319143 | pubmed:abstractText | Genetic factors appear to be important in the restenotic process after percutaneous coronary intervention (PCI), as well as in inflammation, a pivotal factor in restenosis. TNFalpha, a key regulator of inflammatory responses, may exert critical influence on the development of restenosis after PCI. The GENetic DEterminants of Restenosis (GENDER) project included 3104 patients who underwent a successful PCI. Systematic genotyping for six polymorphisms in the TNFalpha gene was performed. The role of TNFalpha in restenosis was also assessed in ApoE*3-Leiden mice, TNFalpha knockout mice, and by local delivery of a TNFalpha biosynthesis inhibitor, thalidomide. The -238G-1031T haplotype of the TNFalpha gene increased clinical and angiographic risk of restenosis (P=0.02 and P=0.002, respectively). In a mouse model of reactive stenosis, arterial TNFalpha mRNA was significantly time-dependently up-regulated. Mice lacking TNFalpha or treated locally with thalidomide showed a reduction in reactive stenosis (P=0.01 and P=0.005, respectively). Clinical and preclinical data indicate that TNFalpha plays an important role in restenosis. Therefore, TNFalpha genotype may be used as a risk marker for restenosis and may contribute to individual patient screening prior to PCI in clinical practice. Inhibition of TNFalpha may be an anti-restenotic target strategy. | lld:pubmed |
| pubmed-article:16319143 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16319143 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16319143 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16319143 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:16319143 | pubmed:issn | 1530-6860 | lld:pubmed |
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| pubmed-article:16319143 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:16319143 | pubmed:volume | 19 | lld:pubmed |
| pubmed-article:16319143 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16319143 | pubmed:authorsComplete | Y | lld:pubmed |
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| pubmed-article:16319143 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:16319143 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:16319143 | pubmed:articleTitle | Tumor necrosis factor-alpha plays an important role in restenosis development. | lld:pubmed |
| pubmed-article:16319143 | pubmed:affiliation | Department of Cardiology, Leiden University Medical Center, The Netherlands. | lld:pubmed |
| pubmed-article:16319143 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16319143 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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