Source:http://linkedlifedata.com/resource/pubmed/id/20453494
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2010-6-23
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pubmed:abstractText |
The vasculature plays a key role in the progression of renal damage in aging, with reduction in glomerular and peritubular capillary density and decreased endothelial proliferative response. In this study, we examined the role of angiopoietin-1 (Ang1) in H(2)O(2)-induced senescence in mouse glomerular endothelial cells (MGECs) and the signaling pathway involved.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
1421-9670
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pubmed:author | |
pubmed:copyrightInfo |
2010 S. Karger AG, Basel.
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pubmed:issnType |
Electronic
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pubmed:volume |
31
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
490-500
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pubmed:dateRevised |
2011-8-3
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pubmed:meshHeading |
pubmed-meshheading:20453494-Angiopoietin-1,
pubmed-meshheading:20453494-Animals,
pubmed-meshheading:20453494-Cell Aging,
pubmed-meshheading:20453494-Endothelium, Vascular,
pubmed-meshheading:20453494-Mice,
pubmed-meshheading:20453494-Mitogen-Activated Protein Kinase 3,
pubmed-meshheading:20453494-Receptor, TIE-2,
pubmed-meshheading:20453494-Signal Transduction
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pubmed:year |
2010
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pubmed:articleTitle |
Angiopoietin-1 inhibits mouse glomerular endothelial cell senescence via Tie2 receptor-modulated ERK1/2 signaling.
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pubmed:affiliation |
Huashan Hospital, Institute of Nephrology, Fudan University, Shanghai, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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