| pubmed-article:19581502 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19581502 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:19581502 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
| pubmed-article:19581502 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
| pubmed-article:19581502 | lifeskim:mentions | umls-concept:C0002006 | lld:lifeskim |
| pubmed-article:19581502 | lifeskim:mentions | umls-concept:C0016059 | lld:lifeskim |
| pubmed-article:19581502 | lifeskim:mentions | umls-concept:C0532128 | lld:lifeskim |
| pubmed-article:19581502 | lifeskim:mentions | umls-concept:C1511545 | lld:lifeskim |
| pubmed-article:19581502 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:19581502 | pubmed:dateCreated | 2009-8-20 | lld:pubmed |
| pubmed-article:19581502 | pubmed:abstractText | The molecular mechanism underlying aldosterone/salt-induced cardiovascular injury remains to be defined. This work was undertaken to determine the role of apoptosis signal-regulating kinase 1 (ASK1) in the mechanism underlying aldosterone-induced cardiac injury in vivo. We compared the in vivo effects of 4 weeks of aldosterone/salt treatment on wild-type and ASK1-deficient mice. Aldosterone infusion plus high salt intake in wild-type mice significantly increased blood pressure and urinary albumin excretion and decreased plasma potassium concentrations, and these effects of aldosterone/salt were not affected by ASK1 deficiency. Thus, ASK1 seems to play a minor role in aldosterone-induced hypertension and renal injury. ASK1 deficiency also failed to affect aldosterone-induced cardiac hypertrophy. However, ASK1 deficiency markedly ameliorated aldosterone-induced cardiac injury, eg, the enhancement of cardiac macrophage infiltration, monocyte chemotactic protein 1 expression, interstitial fibrosis, perivascular fibrosis, and transforming growth factor-beta1 and collagen type I expressions. Thus, ASK1 participates in aldosterone-induced cardiac inflammation and fibrosis. Furthermore, the enhancement of NADPH oxidase-mediated cardiac oxidative stress caused by aldosterone infusion was markedly lessened by ASK1 deficiency, which was associated with the significant amelioration by ASK1 deficiency of aldosterone-induced cardiac Nox2 upregulation. Furthermore, aldosterone/salt treatment significantly enhanced cardiac expression of the angiotensin-converting enzyme and angiotensin II type 1 receptor in wild-type mice, whereas the enhancement of these proteins by aldosterone/salt was abolished by ASK1 deficiency. Our results demonstrate that ASK1 is implicated in aldosterone/salt-induced cardiac inflammation and fibrosis through the enhancement of NADPH oxidase-mediated oxidative stress and the upregulation of the cardiac renin-angiotensin system. | lld:pubmed |
| pubmed-article:19581502 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19581502 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19581502 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19581502 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19581502 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19581502 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19581502 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19581502 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:19581502 | pubmed:issn | 1524-4563 | lld:pubmed |
| pubmed-article:19581502 | pubmed:author | pubmed-author:OgawaHisaoH | lld:pubmed |
| pubmed-article:19581502 | pubmed:author | pubmed-author:IchijoHidenor... | lld:pubmed |
| pubmed-article:19581502 | pubmed:author | pubmed-author:TokutomiYoshi... | lld:pubmed |
| pubmed-article:19581502 | pubmed:author | pubmed-author:NakamuraTaish... | lld:pubmed |
| pubmed-article:19581502 | pubmed:author | pubmed-author:KataokaKeiich... | lld:pubmed |
| pubmed-article:19581502 | pubmed:author | pubmed-author:FukudaMasayaM | lld:pubmed |
| pubmed-article:19581502 | pubmed:author | pubmed-author:Kim-Mitsuyama... | lld:pubmed |
| pubmed-article:19581502 | pubmed:author | pubmed-author:DongYi-FeiYF | lld:pubmed |
| pubmed-article:19581502 | pubmed:author | pubmed-author:NakoHisatoH | lld:pubmed |
| pubmed-article:19581502 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19581502 | pubmed:volume | 54 | lld:pubmed |
| pubmed-article:19581502 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19581502 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19581502 | pubmed:pagination | 544-51 | lld:pubmed |
| pubmed-article:19581502 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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| pubmed-article:19581502 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19581502 | pubmed:articleTitle | Critical role of apoptosis signal-regulating kinase 1 in aldosterone/salt-induced cardiac inflammation and fibrosis. | lld:pubmed |
| pubmed-article:19581502 | pubmed:affiliation | Department of Pharmacology and Molecular Therapeutics, Kumamoto University Graduate School of Medical Sciences, 1-1-1 Honjyo, Kumamoto 860-8556, Japan. kimmitsu@gpo.kumamoto-u.ac.jp. | lld:pubmed |
| pubmed-article:19581502 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19581502 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:26408 | entrezgene:pubmed | pubmed-article:19581502 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:19581502 | lld:entrezgene |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:19581502 | lld:pubmed |
