{"@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/1360848664423604352.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.3390/ijms18010174"}},{"identifier":{"@type":"URI","@value":"https://www.mdpi.com/1422-0067/18/1/174/pdf"}},{"identifier":{"@type":"PMID","@value":"28106734"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"Glycative Stress and Its Defense Machinery Glyoxalase 1 in Renal Pathogenesis"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>Chronic kidney disease is a major public health problem around the world. Because the kidney plays a role in reducing glycative stress, renal dysfunction results in increased glycative stress. In turn, glycative stress, especially that due to advanced glycated end products (AGEs) and their precursors such as reactive carbonyl compounds, exacerbates chronic kidney disease and is related to premature aging in chronic kidney disease, whether caused by diabetes mellitus or otherwise. Factors which hinder a sufficient reduction in glycative stress include the inhibition of anti-glycation enzymes (e.g., GLO-1), as well as pathogenically activated endoplasmic reticulum (ER) stress and hypoxia in the kidney. Promising strategies aimed at halting the vicious cycle between chronic kidney disease and increases in glycative stress include the suppression of AGE accumulation in the body and the enhancement of GLO-1 to strengthen the host defense machinery against glycative stress.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1420001326217637760","@type":"Researcher","personIdentifier":[{"@type":"KAKEN_RESEARCHERS","@value":"10780736"},{"@type":"NRID","@value":"1000010780736"},{"@type":"NRID","@value":"9000406031241"},{"@type":"RESEARCHMAP","@value":"https://researchmap.jp/yohyrakawa"}],"foaf:name":[{"@value":"Yosuke Hirakawa"}],"jpcoar:affiliationName":[{"@value":"Division of Nephrology and Endocrinology, The University of Tokyo Graduate School of Medicine, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1420845751140411136","@type":"Researcher","personIdentifier":[{"@type":"KAKEN_RESEARCHERS","@value":"50232509"},{"@type":"NRID","@value":"1000050232509"},{"@type":"NRID","@value":"9000253019093"},{"@type":"NRID","@value":"9000255721566"},{"@type":"NRID","@value":"9000340458286"},{"@type":"NRID","@value":"9000237900913"},{"@type":"NRID","@value":"9000414552812"},{"@type":"NRID","@value":"9000412352512"},{"@type":"NRID","@value":"9000412353192"},{"@type":"NRID","@value":"9000001122081"},{"@type":"NRID","@value":"9000241570262"},{"@type":"NRID","@value":"9000356595936"},{"@type":"NRID","@value":"9000337074688"},{"@type":"NRID","@value":"9000009634903"},{"@type":"NRID","@value":"9000356879079"},{"@type":"NRID","@value":"9000397854764"},{"@type":"NRID","@value":"9000412352989"},{"@type":"NRID","@value":"9000009659348"},{"@type":"NRID","@value":"9000000296238"},{"@type":"NRID","@value":"9000256089849"},{"@type":"NRID","@value":"9000018917008"},{"@type":"NRID","@value":"9000248961102"},{"@type":"NRID","@value":"9000361676865"},{"@type":"RESEARCHMAP","@value":"https://researchmap.jp/read0006853"}],"foaf:name":[{"@value":"Reiko Inagi"}],"jpcoar:affiliationName":[{"@value":"Division of Chronic Kidney Disease (CKD) Pathophysiology, The University of Tokyo Graduate School of Medicine, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan"}]}],"publication":{"publicationIdentifier":[{"@type":"EISSN","@value":"14220067"}],"prism:publicationName":[{"@value":"International Journal of Molecular Sciences"}],"dc:publisher":[{"@value":"MDPI AG"}],"prism:publicationDate":"2017-01-17","prism:volume":"18","prism:number":"1","prism:startingPage":"174"},"reviewed":"false","dcterms:accessRights":"http://purl.org/coar/access_right/c_abf2","dc:rights":["https://creativecommons.org/licenses/by/4.0/"],"url":[{"@id":"https://www.mdpi.com/1422-0067/18/1/174/pdf"}],"createdAt":"2017-01-18","modifiedAt":"2025-10-11","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Glycation%20End%20Products,%20Advanced","dc:title":"Glycation End Products, Advanced"},{"@id":"https://cir.nii.ac.jp/all?q=Lactoylglutathione%20Lyase","dc:title":"Lactoylglutathione Lyase"},{"@id":"https://cir.nii.ac.jp/all?q=Review","dc:title":"Review"},{"@id":"https://cir.nii.ac.jp/all?q=Endoplasmic%20Reticulum%20Stress","dc:title":"Endoplasmic Reticulum Stress"},{"@id":"https://cir.nii.ac.jp/all?q=Kidney","dc:title":"Kidney"},{"@id":"https://cir.nii.ac.jp/all?q=Models,%20Biological","dc:title":"Models, Biological"},{"@id":"https://cir.nii.ac.jp/all?q=Diabetes%20Mellitus","dc:title":"Diabetes Mellitus"},{"@id":"https://cir.nii.ac.jp/all?q=Animals","dc:title":"Animals"},{"@id":"https://cir.nii.ac.jp/all?q=Humans","dc:title":"Humans"},{"@id":"https://cir.nii.ac.jp/all?q=Renal%20Insufficiency,%20Chronic","dc:title":"Renal Insufficiency, Chronic"},{"@id":"https://cir.nii.ac.jp/all?q=Hypoxia","dc:title":"Hypoxia"}],"project":[{"@id":"https://cir.nii.ac.jp/crid/1040000781921976832","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"16K15465"},{"@type":"JGN","@value":"JP16K15465"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16K15465/"}],"notation":[{"@language":"ja","@value":"Dーアミノ酸による蛋白恒常性破綻（小胞体ストレス）の腎臓病における病因論の解明"},{"@language":"en","@value":"Pathophysiological role of D-amino acid on proteostasis in the kidney"}]},{"@id":"https://cir.nii.ac.jp/crid/1040282256844487808","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"15KT0088"},{"@type":"JGN","@value":"JP15KT0088"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-15KT0088/"}],"notation":[{"@language":"ja","@value":"腎臓老化における小胞体ストレスシグナル（UPR経路）のエピゲノム制御の解明"},{"@language":"en","@value":"Epigenetic regulation of endoplasmic reticulum stress signal in aging of 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