pubmed-article:17404160 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17404160 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:17404160 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:17404160 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:17404160 | lifeskim:mentions | umls-concept:C0014822 | lld:lifeskim |
pubmed-article:17404160 | lifeskim:mentions | umls-concept:C0242698 | lld:lifeskim |
pubmed-article:17404160 | lifeskim:mentions | umls-concept:C0033095 | lld:lifeskim |
pubmed-article:17404160 | lifeskim:mentions | umls-concept:C0205227 | lld:lifeskim |
pubmed-article:17404160 | pubmed:issue | 15 | lld:pubmed |
pubmed-article:17404160 | pubmed:dateCreated | 2007-4-17 | lld:pubmed |
pubmed-article:17404160 | pubmed:abstractText | Erythropoietin (Epo) receptors (EpoRs) are expressed in the heart. We have recently demonstrated that the endogenous Epo-EpoR system plays an important protective role in myocardial ischemia in mice and humans. In the present study, we tested our hypothesis that the endogenous Epo-EpoR system in nonhematopoietic cells also plays a protective role against pressure overload-induced cardiac dysfunction in vivo. | lld:pubmed |
pubmed-article:17404160 | pubmed:language | eng | lld:pubmed |
pubmed-article:17404160 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17404160 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:17404160 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17404160 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17404160 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17404160 | pubmed:month | Apr | lld:pubmed |
pubmed-article:17404160 | pubmed:issn | 1524-4539 | lld:pubmed |
pubmed-article:17404160 | pubmed:author | pubmed-author:TadaHirokoH | lld:pubmed |
pubmed-article:17404160 | pubmed:author | pubmed-author:ShimokawaHiro... | lld:pubmed |
pubmed-article:17404160 | pubmed:author | pubmed-author:KagayaYutakaY | lld:pubmed |
pubmed-article:17404160 | pubmed:author | pubmed-author:ShiratoKunioK | lld:pubmed |
pubmed-article:17404160 | pubmed:author | pubmed-author:OhtaJunJ | lld:pubmed |
pubmed-article:17404160 | pubmed:author | pubmed-author:MinegishiNaok... | lld:pubmed |
pubmed-article:17404160 | pubmed:author | pubmed-author:TakedaMorihik... | lld:pubmed |
pubmed-article:17404160 | pubmed:author | pubmed-author:ItoKentaK | lld:pubmed |
pubmed-article:17404160 | pubmed:author | pubmed-author:AsaumiYasuhid... | lld:pubmed |
pubmed-article:17404160 | pubmed:author | pubmed-author:YamaguchiNobu... | lld:pubmed |
pubmed-article:17404160 | pubmed:author | pubmed-author:ShirotoTakash... | lld:pubmed |
pubmed-article:17404160 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:17404160 | pubmed:day | 17 | lld:pubmed |
pubmed-article:17404160 | pubmed:volume | 115 | lld:pubmed |
pubmed-article:17404160 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17404160 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17404160 | pubmed:pagination | 2022-32 | lld:pubmed |
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pubmed-article:17404160 | pubmed:meshHeading | pubmed-meshheading:17404160... | lld:pubmed |
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pubmed-article:17404160 | pubmed:meshHeading | pubmed-meshheading:17404160... | lld:pubmed |
pubmed-article:17404160 | pubmed:meshHeading | pubmed-meshheading:17404160... | lld:pubmed |
pubmed-article:17404160 | pubmed:meshHeading | pubmed-meshheading:17404160... | lld:pubmed |
pubmed-article:17404160 | pubmed:meshHeading | pubmed-meshheading:17404160... | lld:pubmed |
pubmed-article:17404160 | pubmed:meshHeading | pubmed-meshheading:17404160... | lld:pubmed |
pubmed-article:17404160 | pubmed:meshHeading | pubmed-meshheading:17404160... | lld:pubmed |
pubmed-article:17404160 | pubmed:meshHeading | pubmed-meshheading:17404160... | lld:pubmed |
pubmed-article:17404160 | pubmed:meshHeading | pubmed-meshheading:17404160... | lld:pubmed |
pubmed-article:17404160 | pubmed:meshHeading | pubmed-meshheading:17404160... | lld:pubmed |
pubmed-article:17404160 | pubmed:meshHeading | pubmed-meshheading:17404160... | lld:pubmed |
pubmed-article:17404160 | pubmed:meshHeading | pubmed-meshheading:17404160... | lld:pubmed |
pubmed-article:17404160 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17404160 | pubmed:articleTitle | Protective role of endogenous erythropoietin system in nonhematopoietic cells against pressure overload-induced left ventricular dysfunction in mice. | lld:pubmed |
pubmed-article:17404160 | pubmed:affiliation | Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-Machi, Aoba-Ku, Sendai 980-8574, Japan. | lld:pubmed |
pubmed-article:17404160 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17404160 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:13857 | entrezgene:pubmed | pubmed-article:17404160 | lld:entrezgene |
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