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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2004-3-8
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pubmed:abstractText |
Chronic inflammatory processes might be involved in the progression and destabilization of atherosclerotic plaques. Therefore, identification of the mechanism underlying arterial inflammatory function might lead to the development of novel therapeutic strategies. Angiotensin II (AngII) is implicated in atherogenesis by activating the vascular inflammation system, mainly through monocyte chemotaxis. Therefore, we hypothesized that AngII increases plaque size and promotes destabilization of established atheromas by activating the monocyte chemoattractant protein-1 (MCP-1) pathway.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II Type 1 Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoproteins E,
http://linkedlifedata.com/resource/pubmed/chemical/Ccl2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL2,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Imidazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Inflammation Mediators,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrazoles,
http://linkedlifedata.com/resource/pubmed/chemical/olmesartan medoxomil
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1524-4636
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
24
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
534-9
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:14739122-Angiotensin II,
pubmed-meshheading:14739122-Angiotensin II Type 1 Receptor Blockers,
pubmed-meshheading:14739122-Animals,
pubmed-meshheading:14739122-Aortic Diseases,
pubmed-meshheading:14739122-Apolipoproteins E,
pubmed-meshheading:14739122-Arteriosclerosis,
pubmed-meshheading:14739122-Chemokine CCL2,
pubmed-meshheading:14739122-Chemokines,
pubmed-meshheading:14739122-Cytokines,
pubmed-meshheading:14739122-Disease Progression,
pubmed-meshheading:14739122-Gene Expression Regulation,
pubmed-meshheading:14739122-Gene Targeting,
pubmed-meshheading:14739122-Humans,
pubmed-meshheading:14739122-Hyperlipoproteinemia Type II,
pubmed-meshheading:14739122-Imidazoles,
pubmed-meshheading:14739122-Inflammation,
pubmed-meshheading:14739122-Inflammation Mediators,
pubmed-meshheading:14739122-Injections, Intramuscular,
pubmed-meshheading:14739122-Male,
pubmed-meshheading:14739122-Mice,
pubmed-meshheading:14739122-Mice, Inbred C57BL,
pubmed-meshheading:14739122-Mice, Knockout,
pubmed-meshheading:14739122-Random Allocation,
pubmed-meshheading:14739122-Recombinant Fusion Proteins,
pubmed-meshheading:14739122-Sequence Deletion,
pubmed-meshheading:14739122-Single-Blind Method,
pubmed-meshheading:14739122-Tetrazoles
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pubmed:year |
2004
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pubmed:articleTitle |
Monocyte chemoattractant protein-1 is an essential inflammatory mediator in angiotensin II-induced progression of established atherosclerosis in hypercholesterolemic mice.
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pubmed:affiliation |
Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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