| http://purl.uniprot.org/citations/19581502 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/19581502 | http://www.w3.org/2000/01/rdf-schema#comment | "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."xsd:string |
| http://purl.uniprot.org/citations/19581502 | http://purl.org/dc/terms/identifier | "doi:10.1161/hypertensionaha.109.135392"xsd:string |
| http://purl.uniprot.org/citations/19581502 | http://purl.uniprot.org/core/author | "Fukuda M."xsd:string |
| http://purl.uniprot.org/citations/19581502 | http://purl.uniprot.org/core/author | "Kataoka K."xsd:string |
| http://purl.uniprot.org/citations/19581502 | http://purl.uniprot.org/core/author | "Nakamura T."xsd:string |
| http://purl.uniprot.org/citations/19581502 | http://purl.uniprot.org/core/author | "Ogawa H."xsd:string |
| http://purl.uniprot.org/citations/19581502 | http://purl.uniprot.org/core/author | "Ichijo H."xsd:string |
| http://purl.uniprot.org/citations/19581502 | http://purl.uniprot.org/core/author | "Kim-Mitsuyama S."xsd:string |
| http://purl.uniprot.org/citations/19581502 | http://purl.uniprot.org/core/author | "Tokutomi Y."xsd:string |
| http://purl.uniprot.org/citations/19581502 | http://purl.uniprot.org/core/author | "Nako H."xsd:string |
| http://purl.uniprot.org/citations/19581502 | http://purl.uniprot.org/core/author | "Dong Y.F."xsd:string |
| http://purl.uniprot.org/citations/19581502 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
| http://purl.uniprot.org/citations/19581502 | http://purl.uniprot.org/core/name | "Hypertension"xsd:string |
| http://purl.uniprot.org/citations/19581502 | http://purl.uniprot.org/core/pages | "544-551"xsd:string |
| http://purl.uniprot.org/citations/19581502 | http://purl.uniprot.org/core/title | "Critical role of apoptosis signal-regulating kinase 1 in aldosterone/salt-induced cardiac inflammation and fibrosis."xsd:string |
| http://purl.uniprot.org/citations/19581502 | http://purl.uniprot.org/core/volume | "54"xsd:string |
| http://purl.uniprot.org/citations/19581502 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/19581502 |
| http://purl.uniprot.org/citations/19581502 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/19581502 |
| http://purl.uniprot.org/uniprot/#_A0A1L1ST18-mappedCitation-19581502 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19581502 |
| http://purl.uniprot.org/uniprot/#_D3YVC4-mappedCitation-19581502 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19581502 |
| http://purl.uniprot.org/uniprot/#_D3Z5H1-mappedCitation-19581502 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19581502 |
| http://purl.uniprot.org/uniprot/#_E9PWG9-mappedCitation-19581502 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19581502 |
| http://purl.uniprot.org/uniprot/#_Q14AY4-mappedCitation-19581502 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19581502 |
| http://purl.uniprot.org/uniprot/#_O35099-mappedCitation-19581502 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19581502 |