| pubmed-article:17761193 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17761193 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
| pubmed-article:17761193 | lifeskim:mentions | umls-concept:C0003009 | lld:lifeskim |
| pubmed-article:17761193 | lifeskim:mentions | umls-concept:C0004153 | lld:lifeskim |
| pubmed-article:17761193 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:17761193 | lifeskim:mentions | umls-concept:C0041904 | lld:lifeskim |
| pubmed-article:17761193 | lifeskim:mentions | umls-concept:C0699748 | lld:lifeskim |
| pubmed-article:17761193 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:17761193 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:17761193 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
| pubmed-article:17761193 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:17761193 | pubmed:dateCreated | 2007-10-1 | lld:pubmed |
| pubmed-article:17761193 | pubmed:abstractText | The receptor for advanced glycation end products (RAGE) and the angiotensin II type I receptor (AT1R) have been separately linked to the pathogenesis of diabetic atherosclerosis. However, no prior study has addressed a linkage between RAGE and AT1R in diabetic atherogenesis. Therefore, we tested the hypothesis that upregulation of the ligand-RAGE axis via AT1R is an essential process underlying the disease. Diabetes was induced in apolipoprotein E-deficient (ApoE(-/-)) mice by streptozotocin, and diabetic mice were treated with AT1 receptor blocker (ARB) for 6 weeks. Diabetic ApoE(-/-) mice that were AT1R-deficient (ApoE(-/-)AT1aR(-/-)) were also investigated. In diabetic ApoE(-/-) mice, AT1R was found to increase within 1 week of diabetes induction, before ligand-RAGE pathway activation and other inflammatory changes were observed. Both ARB treatment and AT1aR deficiency suppressed diabetic atherosclerosis, ligand-RAGE expression and inflammatory changes. In contrast, upregulation of the ligand-RAGE pathway was noted in atherosclerotic plaques from non-diabetic ApoE(-/-) mice infused with angiotensin II. In cultured vascular smooth muscle cells, angiotensin II increased RAGE protein levels via AT1R stimulation. Upregulation of the ligand-RAGE pathway via AT1R is an essential mechanism in diabetic atherosclerosis, implying that ARB might decrease diabetic atherogenesis by inhibiting ligand-RAGE signals. | lld:pubmed |
| pubmed-article:17761193 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17761193 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17761193 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17761193 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17761193 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17761193 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17761193 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17761193 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17761193 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:17761193 | pubmed:issn | 0022-2828 | lld:pubmed |
| pubmed-article:17761193 | pubmed:author | pubmed-author:EgashiraKensu... | lld:pubmed |
| pubmed-article:17761193 | pubmed:author | pubmed-author:IwaiMasaruM | lld:pubmed |
| pubmed-article:17761193 | pubmed:author | pubmed-author:HoriuchiMasat... | lld:pubmed |
| pubmed-article:17761193 | pubmed:author | pubmed-author:YamagishiSho-... | lld:pubmed |
| pubmed-article:17761193 | pubmed:author | pubmed-author:ZhaoGangG | lld:pubmed |
| pubmed-article:17761193 | pubmed:author | pubmed-author:SunagawaKenji... | lld:pubmed |
| pubmed-article:17761193 | pubmed:author | pubmed-author:OhtaniKishoK | lld:pubmed |
| pubmed-article:17761193 | pubmed:author | pubmed-author:NakanoKakuK | lld:pubmed |
| pubmed-article:17761193 | pubmed:author | pubmed-author:IharaYoshikoY | lld:pubmed |
| pubmed-article:17761193 | pubmed:author | pubmed-author:KogaJun-ichir... | lld:pubmed |
| pubmed-article:17761193 | pubmed:author | pubmed-author:KuboMitsukiM | lld:pubmed |
| pubmed-article:17761193 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17761193 | pubmed:volume | 43 | lld:pubmed |
| pubmed-article:17761193 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17761193 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17761193 | pubmed:pagination | 455-64 | lld:pubmed |
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| pubmed-article:17761193 | pubmed:meshHeading | pubmed-meshheading:17761193... | lld:pubmed |
| pubmed-article:17761193 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17761193 | pubmed:articleTitle | Upregulation of the ligand-RAGE pathway via the angiotensin II type I receptor is essential in the pathogenesis of diabetic atherosclerosis. | lld:pubmed |
| pubmed-article:17761193 | pubmed:affiliation | Department of Cardiovascular Medicine, Graduate School of Medical Science, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. | lld:pubmed |
| pubmed-article:17761193 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17761193 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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