{"@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/1360021390744198016.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1038/s41598-023-49684-z"}},{"identifier":{"@type":"URI","@value":"https://www.nature.com/articles/s41598-023-49684-z.pdf"}},{"identifier":{"@type":"URI","@value":"https://www.nature.com/articles/s41598-023-49684-z"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"Progression of albuminuria and podocyte injury in focal segmental glomerulosclerosis inhibited by enhanced glycosphingolipid GM3 via valproic acid"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:title>Abstract</jats:title><jats:p>Focal segmental glomerulosclerosis, characterized by decreased numbers of podocytes in glomeruli, is a common cause of refractory nephrotic syndrome. Recently, we showed that enhanced glycosphingolipid GM3 expression after administration of valproic acid, an upregulator of <jats:italic>ST3GAL5/St3gal5</jats:italic>, was effective in preventing albuminuria and podocyte injury. We also revealed the molecular mechanism for this preventive effect, which involves GM3 directly binding nephrin that then act together in glycolipid-enriched membrane (GEM) fractions under normal conditions and in non-GEM fractions under nephrin injury conditions. Kidney disease is frequently referred to as a “silent killer” because it is often difficult to detect subjective symptoms. Thus, primary treatment for these diseases is initiated after the onset of disease progression. Consequently, the efficacy of enhanced levels of GM3 induced by valproic acid needs to be evaluated after the onset of the disease with severe albuminuria such as focal segmental glomerulosclerosis. Here, we report the therapeutic effect of enhanced GM3 expression induced via administration of valproic acid on albuminuria and podocyte injury after the onset focal segmental glomerulosclerosis in anti-nephrin antibody treated mice. Our findings suggest elevated levels of GM3 following treatment with valproic acid has therapeutic utility for kidney disease associated with severe albuminuria and podocyte injury.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380021390744197888","@type":"Researcher","foaf:name":[{"@value":"Nagako Kawashima"}]},{"@id":"https://cir.nii.ac.jp/crid/1420564276185008768","@type":"Researcher","personIdentifier":[{"@type":"KAKEN_RESEARCHERS","@value":"40365101"},{"@type":"NRID","@value":"1000040365101"},{"@type":"NRID","@value":"9000016405549"}],"foaf:name":[{"@value":"Shokichi Naito"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390744197889","@type":"Researcher","foaf:name":[{"@value":"Masaki Nagane"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390744198032","@type":"Researcher","foaf:name":[{"@value":"Tadashi Yamashita"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390744198031","@type":"Researcher","foaf:name":[{"@value":"Ken-ichi Nakayama"}]}],"publication":{"publicationIdentifier":[{"@type":"EISSN","@value":"20452322"}],"prism:publicationName":[{"@value":"Scientific Reports"}],"dc:publisher":[{"@value":"Springer Science and Business Media LLC"}],"prism:publicationDate":"2023-12-15","prism:volume":"13","prism:number":"1"},"reviewed":"false","dcterms:accessRights":"http://purl.org/coar/access_right/c_abf2","dc:rights":["https://creativecommons.org/licenses/by/4.0","https://creativecommons.org/licenses/by/4.0"],"url":[{"@id":"https://www.nature.com/articles/s41598-023-49684-z.pdf"},{"@id":"https://www.nature.com/articles/s41598-023-49684-z"}],"createdAt":"2023-12-18","modifiedAt":"2023-12-21","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Science","dc:title":"Science"},{"@id":"https://cir.nii.ac.jp/all?q=Q","dc:title":"Q"},{"@id":"https://cir.nii.ac.jp/all?q=R","dc:title":"R"},{"@id":"https://cir.nii.ac.jp/all?q=Medicine","dc:title":"Medicine"},{"@id":"https://cir.nii.ac.jp/all?q=Article","dc:title":"Article"}],"project":[{"@id":"https://cir.nii.ac.jp/crid/1040282256977306752","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"18K08249"},{"@type":"JGN","@value":"JP18K08249"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18K08249/"}],"notation":[{"@language":"ja","@value":"正常ポドサイトにおける細胞膜分子・糖脂質GM3の重要性"},{"@language":"en","@value":"Importance of glycolipid GM3 on cell membrane of podocytes"}]}],"relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360004236408931712","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"New Anti-Nephrin Antibody Mediated Podocyte Injury Model Using a C57BL/6 Mouse Strain"}]},{"@id":"https://cir.nii.ac.jp/crid/1360017287071610752","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Gangliosides in Podocyte Biology and Disease"}]},{"@id":"https://cir.nii.ac.jp/crid/1360021390749854336","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Enhanced Levels of Glycosphingolipid GM3 Delay the Progression of Diabetic Nephropathy"}]},{"@id":"https://cir.nii.ac.jp/crid/1360292621129794944","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Enhanced insulin sensitivity in mice lacking ganglioside 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