{"@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/1361981471356635392.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1161/01.hyp.0000255636.11931.a2"}},{"identifier":{"@type":"URI","@value":"https://www.ahajournals.org/doi/full/10.1161/01.HYP.0000255636.11931.a2"}},{"identifier":{"@type":"PMID","@value":"17200434"}},{"identifier":{"@type":"NAID","@value":"30024547291"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"Podocyte as the Target for Aldosterone"}],"dcterms:alternative":[{"@value":"Roles of Oxidative Stress and Sgk1"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>Accumulating evidence suggests that mineralocorticoid receptor blockade effectively reduces proteinuria in hypertensive patients. However, the mechanism of the antiproteinuric effect remains elusive. In this study, we investigated the effects of aldosterone on podocyte, a key player of the glomerular filtration barrier. Uninephrectomized rats were continuously infused with aldosterone and fed a high-salt diet. Aldosterone induced proteinuria progressively, associated with blood pressure elevation. Notably, gene expressions of podocyte-associated molecules nephrin and podocin were markedly decreased in aldosterone-infused rats at 2 weeks, with a gradual decrease thereafter. Immunohistochemical studies and electron microscopy confirmed the podocyte damage. Podocyte injury was accompanied by renal reduced nicotinamide-adenine dinucleotide phosphate oxidase activation, increased oxidative stress, and enhanced expression of aldosterone effector kinase Sgk1. Treatment with eplerenone, a selective aldosterone receptor blocker, almost completely prevented podocyte damage and proteinuria, with normalization of elevated reduced nicotinamide-adenine dinucleotide phosphate oxidase activity. In addition, proteinuria, podocyte damage, and Sgk1 upregulation were significantly alleviated by tempol, a membrane-permeable superoxide dismutase, suggesting the pathogenic role of oxidative stress. Although hydralazine treatment almost normalized blood pressure, it failed to improve proteinuria and podocyte damage. In cultured podocytes with consistent expression of mineralocorticoid receptor, aldosterone stimulated membrane translocation of reduced nicotinamide-adenine dinucleotide phosphate oxidase cytosolic components and oxidative stress generation in podocytes. Furthermore, aldosterone enhanced the expression of Sgk1, which was inhibited by mineralocorticoid receptor antagonist and tempol. In conclusion, podocytes are injured at the early stage in aldosterone-infused rats, resulting in the occurrence of proteinuria. Aldosterone can directly modulate podocyte function, possibly through the induction of oxidative stress and Sgk1.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1381981471356635394","@type":"Researcher","foaf:name":[{"@value":"Shigeru Shibata"}],"jpcoar:affiliationName":[{"@value":"From the Department of Nephrology and Endocrinology (S.S., M.N., S.Y., T.F.), University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan; and the Department of Cell Biology (H.K.), Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1420845751152684672","@type":"Researcher","personIdentifier":[{"@type":"KAKEN_RESEARCHERS","@value":"60302733"},{"@type":"NRID","@value":"1000060302733"},{"@type":"NRID","@value":"9000017333350"},{"@type":"NRID","@value":"9000252929275"},{"@type":"NRID","@value":"9000283300791"},{"@type":"NRID","@value":"9000007157269"},{"@type":"NRID","@value":"9000014664129"},{"@type":"NRID","@value":"9000003885209"},{"@type":"NRID","@value":"9000020235902"},{"@type":"NRID","@value":"9000001959317"},{"@type":"NRID","@value":"9000240079610"},{"@type":"NRID","@value":"9000016664949"},{"@type":"NRID","@value":"9000018534181"},{"@type":"NRID","@value":"9000356639244"},{"@type":"NRID","@value":"9000241764878"},{"@type":"NRID","@value":"9000018393676"},{"@type":"NRID","@value":"9000413543384"},{"@type":"NRID","@value":"9000257776721"},{"@type":"NRID","@value":"9000402387221"},{"@type":"NRID","@value":"9000404644736"},{"@type":"NRID","@value":"9000408891603"},{"@type":"NRID","@value":"9000011138237"},{"@type":"NRID","@value":"9000016399279"},{"@type":"RESEARCHMAP","@value":"https://researchmap.jp/00000000"}],"foaf:name":[{"@value":"Miki Nagase"}],"jpcoar:affiliationName":[{"@value":"From the Department of Nephrology and Endocrinology (S.S., M.N., S.Y., T.F.), University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan; and the Department of Cell Biology (H.K.), Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1381981471356635395","@type":"Researcher","foaf:name":[{"@value":"Shigetaka Yoshida"}],"jpcoar:affiliationName":[{"@value":"From the Department of Nephrology and Endocrinology (S.S., M.N., S.Y., T.F.), University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan; and the Department of Cell Biology (H.K.), Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1381981471356635392","@type":"Researcher","foaf:name":[{"@value":"Hiroshi Kawachi"}],"jpcoar:affiliationName":[{"@value":"From the Department of Nephrology and Endocrinology (S.S., M.N., S.Y., T.F.), University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan; and the Department of Cell Biology (H.K.), Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1381981471356635393","@type":"Researcher","foaf:name":[{"@value":"Toshiro Fujita"}],"jpcoar:affiliationName":[{"@value":"From the Department of Nephrology and Endocrinology (S.S., M.N., S.Y., T.F.), University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan; and the Department of Cell Biology (H.K.), Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan."}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"0194911X"},{"@type":"EISSN","@value":"15244563"},{"@type":"PISSN","@value":"http://id.crossref.org/issn/0194911X"}],"prism:publicationName":[{"@value":"Hypertension"}],"dc:publisher":[{"@value":"Ovid Technologies (Wolters Kluwer Health)"}],"prism:publicationDate":"2007-02","prism:volume":"49","prism:number":"2","prism:startingPage":"355","prism:endingPage":"364"},"reviewed":"false","dcterms:accessRights":"http://purl.org/coar/access_right/c_abf2","url":[{"@id":"https://www.ahajournals.org/doi/full/10.1161/01.HYP.0000255636.11931.a2"}],"createdAt":"2007-01-03","modifiedAt":"2024-05-12","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Time%20Factors","dc:title":"Time Factors"},{"@id":"https://cir.nii.ac.jp/all?q=Blood%20Pressure","dc:title":"Blood Pressure"},{"@id":"https://cir.nii.ac.jp/all?q=Protein%20Serine-Threonine%20Kinases","dc:title":"Protein Serine-Threonine Kinases"},{"@id":"https://cir.nii.ac.jp/all?q=Spironolactone","dc:title":"Spironolactone"},{"@id":"https://cir.nii.ac.jp/all?q=Kidney","dc:title":"Kidney"},{"@id":"https://cir.nii.ac.jp/all?q=Nephrectomy","dc:title":"Nephrectomy"},{"@id":"https://cir.nii.ac.jp/all?q=Antioxidants","dc:title":"Antioxidants"},{"@id":"https://cir.nii.ac.jp/all?q=Immediate-Early%20Proteins","dc:title":"Immediate-Early Proteins"},{"@id":"https://cir.nii.ac.jp/all?q=Cyclic%20N-Oxides","dc:title":"Cyclic N-Oxides"},{"@id":"https://cir.nii.ac.jp/all?q=Rats,%20Sprague-Dawley","dc:title":"Rats, Sprague-Dawley"},{"@id":"https://cir.nii.ac.jp/all?q=Animals","dc:title":"Animals"},{"@id":"https://cir.nii.ac.jp/all?q=Aldosterone","dc:title":"Aldosterone"},{"@id":"https://cir.nii.ac.jp/all?q=Antihypertensive%20Agents","dc:title":"Antihypertensive Agents"},{"@id":"https://cir.nii.ac.jp/all?q=Cells,%20Cultured","dc:title":"Cells, Cultured"},{"@id":"https://cir.nii.ac.jp/all?q=Infusion%20Pumps","dc:title":"Infusion Pumps"},{"@id":"https://cir.nii.ac.jp/all?q=Mineralocorticoid%20Receptor%20Antagonists","dc:title":"Mineralocorticoid Receptor Antagonists"},{"@id":"https://cir.nii.ac.jp/all?q=Podocytes","dc:title":"Podocytes"},{"@id":"https://cir.nii.ac.jp/all?q=NADPH%20Oxidases","dc:title":"NADPH Oxidases"},{"@id":"https://cir.nii.ac.jp/all?q=Hydralazine","dc:title":"Hydralazine"},{"@id":"https://cir.nii.ac.jp/all?q=Eplerenone","dc:title":"Eplerenone"},{"@id":"https://cir.nii.ac.jp/all?q=Rats","dc:title":"Rats"},{"@id":"https://cir.nii.ac.jp/all?q=Up-Regulation","dc:title":"Up-Regulation"},{"@id":"https://cir.nii.ac.jp/all?q=Enzyme%20Activation","dc:title":"Enzyme Activation"},{"@id":"https://cir.nii.ac.jp/all?q=Oxidative%20Stress","dc:title":"Oxidative Stress"},{"@id":"https://cir.nii.ac.jp/all?q=Proteinuria","dc:title":"Proteinuria"},{"@id":"https://cir.nii.ac.jp/all?q=Receptors,%20Mineralocorticoid","dc:title":"Receptors, Mineralocorticoid"},{"@id":"https://cir.nii.ac.jp/all?q=Spin%20Labels","dc:title":"Spin Labels"}],"project":[{"@id":"https://cir.nii.ac.jp/crid/1040000781943843840","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"17590820"},{"@type":"JGN","@value":"JP17590820"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-17590820/"}],"notation":[{"@language":"ja","@value":"生活習慣病における糸球体上皮細胞障害機序の解明と蛋白尿抑制の新たな治療戦略の確立"},{"@language":"en","@value":"Glomerular podocyte injury in lifestyle-related disease : elucidation of its mechanism and establishment of novel therapeutic strategy to inhibit proteinuria"}]},{"@id":"https://cir.nii.ac.jp/crid/1040282256960846976","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"18590886"},{"@type":"JGN","@value":"JP18590886"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18590886/"}],"notation":[{"@language":"ja","@value":"蛋白尿発症の分子機構の解析 -蛋白尿抑制治療法の開発-"},{"@language":"en","@value":"Clarification of the pathogenic mechanism of proteinuria"}]}],"relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360002219825942144","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Natriuretic Peptide Receptor Guanylyl Cyclase-A Protects Podocytes from Aldosterone-Induced Glomerular Injury"}]},{"@id":"https://cir.nii.ac.jp/crid/1360004231497863296","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"The Kidneys and Aldosterone/Mineralocorticoid Receptor System in Salt-Sensitive Hypertension"}]},{"@id":"https://cir.nii.ac.jp/crid/1360004232314971776","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"A serine protease inhibitor attenuates aldosterone-induced kidney injuries via the suppression of plasmin 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deletion of guanylyl cyclase-A and p38 mitogen-activated protein kinase in podocytes with aldosterone administration causes glomerular intra-capillary thrombi"}]},{"@id":"https://cir.nii.ac.jp/crid/1360306904407932928","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Involvement of Mineralocorticoid Receptor Activation by High Mobility Group Box 1 and Receptor for Advanced Glycation End Products in the Development of Acute Kidney Injury"}]},{"@id":"https://cir.nii.ac.jp/crid/1360306904420000640","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Recent Advances and Perspectives on the Use of Mineralocorticoid Receptor Antagonists for the Treatment of Hypertension and Chronic Kidney Disease: A Review"}]},{"@id":"https://cir.nii.ac.jp/crid/1360564064063787392","@type":"Article","resourceType":"学術雑誌論文(journal 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Receptor Antagonists for Preventing Chronic Kidney Disease Progression: Current Evidence and Future Challenges"}]},{"@id":"https://cir.nii.ac.jp/crid/1360584339776613248","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Roles of the mechanosensitive ion channel Piezo1 in the renal podocyte injury of experimental hypertensive nephropathy"}]},{"@id":"https://cir.nii.ac.jp/crid/1360588379378715520","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Piezo ion channels: long-sought-after mechanosensors mediating hypertension and hypertensive nephropathy"}]},{"@id":"https://cir.nii.ac.jp/crid/1360846642438488576","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"The Role of Aldosterone in Obesity-Related 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