{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1362825895708487808.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1161/circulationaha.104.525550"}},{"identifier":{"@type":"URI","@value":"https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.104.525550"}},{"identifier":{"@type":"PMID","@value":"16145000"}},{"identifier":{"@type":"NAID","@value":"30022673206"}}],"dc:title":[{"@value":"Deletion of Angiotensin II Type 2 Receptor Exaggerated Atherosclerosis in Apolipoprotein E–Null Mice"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>\n            <jats:bold>\n              <jats:italic>Background—</jats:italic>\n            </jats:bold>\n            The role of angiotensin II (Ang II) type 2 (AT\n            <jats:sub>2</jats:sub>\n            ) receptor in atherosclerosis was explored with the use of AT\n            <jats:sub>2</jats:sub>\n            receptor/apolipoprotein E (ApoE)–double-knockout (AT\n            <jats:sub>2</jats:sub>\n            /ApoE-DKO) mice, with a focus on oxidative stress.\n          </jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Methods and Results—</jats:italic>\n            </jats:bold>\n            After treatment with a high-cholesterol diet (1.25% cholesterol) for 10 weeks, ApoE-knockout (KO) mice developed atherosclerotic lesions in the aorta. In AT\n            <jats:sub>2</jats:sub>\n            /ApoE-DKO mice receiving a high-cholesterol diet, the atherosclerotic changes were further exaggerated, without significant changes in plasma cholesterol level and blood pressure. In the atherosclerotic lesion, an increase in superoxide production, NADPH oxidase activity, and expression of p47\n            <jats:sup>phox</jats:sup>\n            was observed. These changes were also greater in AT\n            <jats:sub>2</jats:sub>\n            /ApoE-DKO mice. An Ang II type 1 (AT\n            <jats:sub>1</jats:sub>\n            ) receptor blocker, valsartan, inhibited atherosclerotic lesion formation, superoxide production, NADPH oxidase activity, and p47\n            <jats:sup>phox</jats:sup>\n            expression; these inhibitory effects were significantly weaker in AT\n            <jats:sub>2</jats:sub>\n            /ApoE-KO mice. We further examined the signaling mechanism of the AT\n            <jats:sub>2</jats:sub>\n            receptor–mediated antioxidative effect in cultured fetal vascular smooth muscle cells. NADPH oxidase activity and phosphorylation and translocation of p47\n            <jats:sup>phox</jats:sup>\n            induced by Ang II were inhibited by valsartan but enhanced by an AT\n            <jats:sub>2</jats:sub>\n            receptor blocker, PD123319.\n          </jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Conclusions—</jats:italic>\n            </jats:bold>\n            These results suggest that AT\n            <jats:sub>2</jats:sub>\n            receptor stimulation attenuates atherosclerosis through inhibition of oxidative stress and that the antiatherosclerotic effect of valsartan could be at least partly due to AT\n            <jats:sub>2</jats:sub>\n            receptor stimulation by unbound Ang II.\n          </jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1382825895708487818","@type":"Researcher","foaf:name":[{"@value":"Masaru Iwai"}],"jpcoar:affiliationName":[{"@value":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology, Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895708487814","@type":"Researcher","foaf:name":[{"@value":"Rui Chen"}],"jpcoar:affiliationName":[{"@value":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology, Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895708487811","@type":"Researcher","foaf:name":[{"@value":"Zhen Li"}],"jpcoar:affiliationName":[{"@value":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology, Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895708487815","@type":"Researcher","foaf:name":[{"@value":"Tetsuya Shiuchi"}],"jpcoar:affiliationName":[{"@value":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology, Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895708487813","@type":"Researcher","foaf:name":[{"@value":"Jun Suzuki"}],"jpcoar:affiliationName":[{"@value":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology, Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895708487812","@type":"Researcher","foaf:name":[{"@value":"Ayumi Ide"}],"jpcoar:affiliationName":[{"@value":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology, Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895708487817","@type":"Researcher","foaf:name":[{"@value":"Masahiro Tsuda"}],"jpcoar:affiliationName":[{"@value":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology, Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895708487809","@type":"Researcher","foaf:name":[{"@value":"Midori Okumura"}],"jpcoar:affiliationName":[{"@value":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology, Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895708487808","@type":"Researcher","foaf:name":[{"@value":"Li-Juan Min"}],"jpcoar:affiliationName":[{"@value":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology, Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895708487816","@type":"Researcher","foaf:name":[{"@value":"Masaki Mogi"}],"jpcoar:affiliationName":[{"@value":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology, Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825895708487810","@type":"Researcher","foaf:name":[{"@value":"Masatsugu Horiuchi"}],"jpcoar:affiliationName":[{"@value":"From the Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology, Ehime University School of Medicine, Shitsukawa, Tohon, Ehime, Japan."}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00097322"},{"@type":"EISSN","@value":"15244539"}],"prism:publicationName":[{"@value":"Circulation"}],"dc:publisher":[{"@value":"Ovid Technologies (Wolters Kluwer Health)"}],"prism:publicationDate":"2005-09-13","prism:volume":"112","prism:number":"11","prism:startingPage":"1636","prism:endingPage":"1643"},"reviewed":"false","dcterms:accessRights":"http://purl.org/coar/access_right/c_abf2","url":[{"@id":"https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.104.525550"}],"createdAt":"2005-09-07","modifiedAt":"2024-05-13","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=rac1%20GTP-Binding%20Protein","dc:title":"rac1 GTP-Binding Protein"},{"@id":"https://cir.nii.ac.jp/all?q=Pyridines","dc:title":"Pyridines"},{"@id":"https://cir.nii.ac.jp/all?q=Myocytes,%20Smooth%20Muscle","dc:title":"Myocytes, Smooth Muscle"},{"@id":"https://cir.nii.ac.jp/all?q=Tetrazoles","dc:title":"Tetrazoles"},{"@id":"https://cir.nii.ac.jp/all?q=Angiotensin%20II%20Type%202%20Receptor%20Blockers","dc:title":"Angiotensin II Type 2 Receptor Blockers"},{"@id":"https://cir.nii.ac.jp/all?q=Receptor,%20Angiotensin,%20Type%202","dc:title":"Receptor, Angiotensin, Type 2"},{"@id":"https://cir.nii.ac.jp/all?q=Muscle,%20Smooth,%20Vascular","dc:title":"Muscle, Smooth, Vascular"},{"@id":"https://cir.nii.ac.jp/all?q=Rats,%20Sprague-Dawley","dc:title":"Rats, Sprague-Dawley"},{"@id":"https://cir.nii.ac.jp/all?q=Mice","dc:title":"Mice"},{"@id":"https://cir.nii.ac.jp/all?q=Apolipoproteins%20E","dc:title":"Apolipoproteins E"},{"@id":"https://cir.nii.ac.jp/all?q=Animals","dc:title":"Animals"},{"@id":"https://cir.nii.ac.jp/all?q=Phosphorylation","dc:title":"Phosphorylation"},{"@id":"https://cir.nii.ac.jp/all?q=Aorta","dc:title":"Aorta"},{"@id":"https://cir.nii.ac.jp/all?q=Cells,%20Cultured","dc:title":"Cells, Cultured"},{"@id":"https://cir.nii.ac.jp/all?q=Mice,%20Knockout","dc:title":"Mice, Knockout"},{"@id":"https://cir.nii.ac.jp/all?q=Angiotensin%20II","dc:title":"Angiotensin II"},{"@id":"https://cir.nii.ac.jp/all?q=Imidazoles","dc:title":"Imidazoles"},{"@id":"https://cir.nii.ac.jp/all?q=NADPH%20Oxidases","dc:title":"NADPH Oxidases"},{"@id":"https://cir.nii.ac.jp/all?q=Valine","dc:title":"Valine"},{"@id":"https://cir.nii.ac.jp/all?q=Atherosclerosis","dc:title":"Atherosclerosis"},{"@id":"https://cir.nii.ac.jp/all?q=Phosphoproteins","dc:title":"Phosphoproteins"},{"@id":"https://cir.nii.ac.jp/all?q=Rats","dc:title":"Rats"},{"@id":"https://cir.nii.ac.jp/all?q=Oxidative%20Stress","dc:title":"Oxidative Stress"},{"@id":"https://cir.nii.ac.jp/all?q=Valsartan","dc:title":"Valsartan"},{"@id":"https://cir.nii.ac.jp/all?q=Proto-Oncogene%20Proteins%20c-akt","dc:title":"Proto-Oncogene Proteins c-akt"},{"@id":"https://cir.nii.ac.jp/all?q=Gene%20Deletion","dc:title":"Gene Deletion"}],"relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360285711407628800","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Deletion of the Angiotensin II Type 1a Receptor Prevents Atherosclerotic Plaque Rupture in Apolipoprotein E\n            <sup>−/−</sup>\n            Mice"}]},{"@id":"https://cir.nii.ac.jp/crid/1360567182301994752","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Reciprocal regulation of cholesterol excretion in apolipoprotein E-null mice by angiotensin II type 1 and type 2 receptor deficiency"}]},{"@id":"https://cir.nii.ac.jp/crid/1360567185888467328","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Synergistic Inhibitory Effect of Rosuvastatin and Angiotensin II Type 2 Receptor Agonist on Vascular Remodeling"}]},{"@id":"https://cir.nii.ac.jp/crid/1360848662531057408","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Enhancement of Adipocyte Browning by Angiotensin II Type 1 Receptor Blockade"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001204431775616","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"RhoA and Rac1 Changes in the Atherosclerotic Lesions of WHHLMI Rabbits"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001205256481664","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Chronic inflammation and atherosclerosis : A critical role for renin angiotensin system that is activated by lifestyle-related diseases"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001206297376512","@type":"Article","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Signaling Crosstalk Angiotensin II Receptor Subtypes and Insulin"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001288033985152","@type":"Article","relationType":["isReferencedBy","isCitedBy"],"jpcoar:relatedTitle":[{"@language":"ja","@value":"心不全研究の進歩(循環器学2005年の進歩)"}]},{"@id":"https://cir.nii.ac.jp/crid/1390282679220146304","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Crucial role of renin-angiotensin system in the pathogenesis of atherosclerosis"}]},{"@id":"https://cir.nii.ac.jp/crid/1390282681422381184","@type":"Article","relationType":["isReferencedBy","isCitedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Disease state and treatment of renin angiotensin system. 4) The significance of RAS suppression in the formation of  arterioscleosis"},{"@language":"ja","@value":"レニン・アンジオテンシン系の病態と治療　　４）動脈硬化形成におけるＲＡＳの意義"},{"@value":"動脈硬化形成におけるRASの意義"},{"@language":"ja-Kana","@value":"ドウミャク コウカ ケイセイ ニ オケル RAS ノ イギ"}]},{"@id":"https://cir.nii.ac.jp/crid/1571980075280392192","@type":"Article","relationType":["isCitedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Role of NAD(P)H Oxidase and Its Regulation in Chronic Hypertension"}]},{"@id":"https://cir.nii.ac.jp/crid/1572824500220820224","@type":"Article","relationType":["isCitedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Regression of Atherosclerosis by Amlodipine via Anti-Inflammatory and Anti-Oxidative Stress Actions"}]},{"@id":"https://cir.nii.ac.jp/crid/2050588892097690880","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Olmesartan protects endothelial cells against oxidative stress-mediated cellular injury"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.1161/circulationaha.104.525550"},{"@type":"CIA","@value":"30022673206"},{"@type":"OPENAIRE","@value":"doi_dedup___::53f39bd65a49f48fc89e1fd988644363"},{"@type":"CROSSREF","@value":"10.2152/jmi.57.12_references_DOI_JDc0F6DVApxVlg5fNO3NH8adwNJ"},{"@type":"CROSSREF","@value":"10.1507/endocrj.53.1_references_DOI_JDc0F6DVApxVlg5fNO3NH8adwNJ"},{"@type":"CROSSREF","@value":"10.1253/jjcsc.14.1_110_references_DOI_JDc0F6DVApxVlg5fNO3NH8adwNJ"},{"@type":"CROSSREF","@value":"10.1161/atvbaha.112.249516_references_DOI_7SkAh6WA6o3b5FS14VF0T7B26LD"},{"@type":"CROSSREF","@value":"10.5551/jat.2394_references_DOI_JDc0F6DVApxVlg5fNO3NH8adwNJ"},{"@type":"CROSSREF","@value":"10.1016/j.lfs.2012.12.006_references_DOI_JDc0F6DVApxVlg5fNO3NH8adwNJ"},{"@type":"CROSSREF","@value":"10.1124/jpet.116.233148_references_DOI_JDc0F6DVApxVlg5fNO3NH8adwNJ"},{"@type":"CROSSREF","@value":"10.1007/s10157-015-1111-5_references_DOI_JDc0F6DVApxVlg5fNO3NH8adwNJ"},{"@type":"CROSSREF","@value":"10.1371/journal.pone.0167704_references_DOI_JDc0F6DVApxVlg5fNO3NH8adwNJ"},{"@type":"CROSSREF","@value":"10.2169/naika.95.1762_references_DOI_JDc0F6DVApxVlg5fNO3NH8adwNJ"},{"@type":"CROSSREF","@value":"10.2492/inflammregen.31.245_references_DOI_JDc0F6DVApxVlg5fNO3NH8adwNJ"}]}