| pubmed-article:18061195 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18061195 | lifeskim:mentions | umls-concept:C0011849 | lld:lifeskim |
| pubmed-article:18061195 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:18061195 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:18061195 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:18061195 | lifeskim:mentions | umls-concept:C0063164 | lld:lifeskim |
| pubmed-article:18061195 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:18061195 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:18061195 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:18061195 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:18061195 | pubmed:dateCreated | 2008-3-31 | lld:pubmed |
| pubmed-article:18061195 | pubmed:abstractText | HMG-CoA reductase inhibitors have been shown to upregulate GTP cyclohydrolase I (GTPCH-I), the key enzyme for tetrahydrobiopterin de novo synthesis and to normalize tetrahydrobiopterin levels in hyperglycemic endothelial cells. We sought to determine whether in vivo treatment with the HMG-CoA reductase inhibitor atorvastatin is able to upregulate the GTPCH-I, to recouple eNOS and to normalize endothelial dysfunction in an experimental model of diabetes mellitus. | lld:pubmed |
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| pubmed-article:18061195 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18061195 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18061195 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18061195 | pubmed:month | May | lld:pubmed |
| pubmed-article:18061195 | pubmed:issn | 1879-1484 | lld:pubmed |
| pubmed-article:18061195 | pubmed:author | pubmed-author:XuJianJ | lld:pubmed |
| pubmed-article:18061195 | pubmed:author | pubmed-author:ZouMing-HuiMH | lld:pubmed |
