| pubmed-article:17707356 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17707356 | lifeskim:mentions | umls-concept:C1522564 | lld:lifeskim |
| pubmed-article:17707356 | lifeskim:mentions | umls-concept:C1417947 | lld:lifeskim |
| pubmed-article:17707356 | lifeskim:mentions | umls-concept:C1442161 | lld:lifeskim |
| pubmed-article:17707356 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:17707356 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:17707356 | pubmed:dateCreated | 2007-10-15 | lld:pubmed |
| pubmed-article:17707356 | pubmed:abstractText | Chronic ischemia is associated with alterations in genes that result in myocardial remodeling. An important biochemical basis of cardiac remodeling is generation of reactive oxygen species (ROS). A few studies have suggested that acute ischemia triggers signals for remodeling. We examined the hypothesis that targeted deletion of lectin-like oxidized-LDL receptor (LOX-1) may inhibit signals related to cardiac remodeling. | lld:pubmed |
| pubmed-article:17707356 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17707356 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17707356 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17707356 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17707356 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17707356 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17707356 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17707356 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17707356 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17707356 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17707356 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17707356 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:17707356 | pubmed:issn | 0008-6363 | lld:pubmed |
| pubmed-article:17707356 | pubmed:author | pubmed-author:SuzukiHiroshi... | lld:pubmed |
| pubmed-article:17707356 | pubmed:author | pubmed-author:InoueNobutaka... | lld:pubmed |
| pubmed-article:17707356 | pubmed:author | pubmed-author:KawaseYosukeY | lld:pubmed |
| pubmed-article:17707356 | pubmed:author | pubmed-author:JishageKou-ic... | lld:pubmed |
| pubmed-article:17707356 | pubmed:author | pubmed-author:SawamuraTatsu... | lld:pubmed |
| pubmed-article:17707356 | pubmed:author | pubmed-author:MehtaJawahar... | lld:pubmed |
| pubmed-article:17707356 | pubmed:author | pubmed-author:FujitaYoshiko... | lld:pubmed |
| pubmed-article:17707356 | pubmed:author | pubmed-author:JiaweiChenC | lld:pubmed |
| pubmed-article:17707356 | pubmed:author | pubmed-author:DandapatAbhij... | lld:pubmed |
| pubmed-article:17707356 | pubmed:author | pubmed-author:HuChangpingC | lld:pubmed |
| pubmed-article:17707356 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17707356 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:17707356 | pubmed:volume | 76 | lld:pubmed |
| pubmed-article:17707356 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17707356 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17707356 | pubmed:pagination | 292-302 | lld:pubmed |
| pubmed-article:17707356 | pubmed:meshHeading | pubmed-meshheading:17707356... | lld:pubmed |
| pubmed-article:17707356 | pubmed:meshHeading | pubmed-meshheading:17707356... | lld:pubmed |
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| pubmed-article:17707356 | pubmed:meshHeading | pubmed-meshheading:17707356... | lld:pubmed |
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| pubmed-article:17707356 | pubmed:meshHeading | pubmed-meshheading:17707356... | lld:pubmed |
| pubmed-article:17707356 | pubmed:meshHeading | pubmed-meshheading:17707356... | lld:pubmed |
| pubmed-article:17707356 | pubmed:meshHeading | pubmed-meshheading:17707356... | lld:pubmed |
| pubmed-article:17707356 | pubmed:meshHeading | pubmed-meshheading:17707356... | lld:pubmed |
| pubmed-article:17707356 | pubmed:meshHeading | pubmed-meshheading:17707356... | lld:pubmed |
| pubmed-article:17707356 | pubmed:meshHeading | pubmed-meshheading:17707356... | lld:pubmed |
| pubmed-article:17707356 | pubmed:meshHeading | pubmed-meshheading:17707356... | lld:pubmed |
| pubmed-article:17707356 | pubmed:meshHeading | pubmed-meshheading:17707356... | lld:pubmed |
| pubmed-article:17707356 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17707356 | pubmed:articleTitle | LOX-1 deletion alters signals of myocardial remodeling immediately after ischemia-reperfusion. | lld:pubmed |
| pubmed-article:17707356 | pubmed:affiliation | Department of Internal Medicine, University of Arkansas for Medical Sciences, Central Arkansas Veterans Healthcare System, Little Rock, AR 72205-7199, USA. | lld:pubmed |
| pubmed-article:17707356 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17707356 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:17707356 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:108078 | entrezgene:pubmed | pubmed-article:17707356 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:17707356 | lld:entrezgene |
