=== Generating (published_papers) ===
=== Generating (teaching_experience) ===
=== Generating (misc) ===
=== Generating (research_projects) ===
=== Generating (presentations) ===
==== begin registerFile(/WWW/pub2/data/ERD/person/376686/researchmap/published_papers.jsonl) ====
line:1, {"insert":{"user_id":"6000007612","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/119529","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/38928090","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=410124","label":"url"}],"paper_title":{"en":"Deficiency Causes Mitoribosome Excess in Diabetic Nephropathy Mediated by Transcriptional Repressor HIC1.","ja":"Deficiency Causes Mitoribosome Excess in Diabetic Nephropathy Mediated by Transcriptional Repressor HIC1."},"authors":{"en":[{"name":"Hasegawa Kazuhiro"},{"name":"Tamaki Masanori"},{"name":"Sakamaki Yusuke"},{"name":"Wakino Shu"}],"ja":[{"name":"長谷川 一宏"},{"name":"田蒔 昌憲"},{"name":"Sakamaki Yusuke"},{"name":"𦚰野 修"}]},"description":{"en":"overexpression preserved mitoribosomal function, suggesting its protective role in DN.","ja":"overexpression preserved mitoribosomal function, suggesting its protective role in DN."},"publication_date":"2024-06-09","publication_name":{"en":"International Journal of Molecular Sciences","ja":"International Journal of Molecular Sciences"},"volume":"Vol.25","number":"No.12","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3390/ijms25126384"],"issn":["1422-0067"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:2, {"insert":{"user_id":"6000007612","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/119528","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/38587753","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=410122","label":"url"}],"paper_title":{"en":"Ability of NAD and Sirt1 to epigenetically suppress albuminuria.","ja":"Ability of NAD and Sirt1 to epigenetically suppress albuminuria."},"authors":{"en":[{"name":"Hasegawa Kazuhiro"},{"name":"Tamaki Masanori"},{"name":"Shibata Eriko"},{"name":"Inagaki Taizo"},{"name":"Minato Masanori"},{"name":"Yamaguchi Sumiyo"},{"name":"Shimizu Ikuko"},{"name":"Miyakami Shinji"},{"name":"Tada Miho"},{"name":"Wakino Shu"}],"ja":[{"name":"長谷川 一宏"},{"name":"田蒔 昌憲"},{"name":"柴田 恵理子"},{"name":"稲垣 太造"},{"name":"湊 将典"},{"name":"Yamaguchi Sumiyo"},{"name":"清水 郁子"},{"name":"Miyakami Shinji"},{"name":"多田 美穂"},{"name":"𦚰野 修"}]},"description":{"en":"The time for diabetic nephropathy (DN) to progress from mild to severe is long. Thus, methods to continuously repress DN are required to exert long-lasting effects mediated through epigenetic regulation. In this study, we demonstrated the ability of nicotinamide adenine dinucleotide (NAD) and its metabolites to reduce albuminuria through Sirt1- or Nampt-dependent epigenetic regulation. We previously reported that proximal tubular Sirt1 was lowered before glomerular Sirt1. Repressed glomerular Sirt1 was found to epigenetically elevate Claudin-1. In addition, we reported that proximal tubular Nampt deficiency epigenetically augmented TIMP-1 levels in Sirt6-mediated pathways, leading to type-IV collagen deposition and diabetic fibrosis. Altogether, we propose that the Sirt1/Claudin-1 axis may be crucial in the onset of albuminuria at the early stages of DN and that the Nampt/Sirt6/TIMP-1 axis promotes diabetic fibrosis in the middle to late stages of DN. Finally, administration of NMN, an NAD precursor, epigenetically potentiates the regression of the onset of DN to maintain Sirt1 and repress Claudin-1 in podocytes, suggesting the potential use of NAD metabolites as epigenetic medications for DN.","ja":"The time for diabetic nephropathy (DN) to progress from mild to severe is long. Thus, methods to continuously repress DN are required to exert long-lasting effects mediated through epigenetic regulation. In this study, we demonstrated the ability of nicotinamide adenine dinucleotide (NAD) and its metabolites to reduce albuminuria through Sirt1- or Nampt-dependent epigenetic regulation. We previously reported that proximal tubular Sirt1 was lowered before glomerular Sirt1. Repressed glomerular Sirt1 was found to epigenetically elevate Claudin-1. In addition, we reported that proximal tubular Nampt deficiency epigenetically augmented TIMP-1 levels in Sirt6-mediated pathways, leading to type-IV collagen deposition and diabetic fibrosis. Altogether, we propose that the Sirt1/Claudin-1 axis may be crucial in the onset of albuminuria at the early stages of DN and that the Nampt/Sirt6/TIMP-1 axis promotes diabetic fibrosis in the middle to late stages of DN. Finally, administration of NMN, an NAD precursor, epigenetically potentiates the regression of the onset of DN to maintain Sirt1 and repress Claudin-1 in podocytes, suggesting the potential use of NAD metabolites as epigenetic medications for DN."},"publication_date":"2024-04-08","publication_name":{"en":"Clinical and Experimental Nephrology","ja":"Clinical and Experimental Nephrology"},"volume":"Vol.28","number":"No.7","starting_page":"599","ending_page":"607","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s10157-024-02502-w"],"issn":["1437-7799"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
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==== end registerFile(/WWW/pub2/data/ERD/person/376686/researchmap/published_papers.jsonl, N-cB-ZIBwbWENEENIF_p) ====
==== begin registerFile(/WWW/pub2/data/ERD/person/376686/researchmap/misc.jsonl) ====
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==== end registerFile(/WWW/pub2/data/ERD/person/376686/researchmap/misc.jsonl, OecB-ZIBwbWENEENIV9o) ====
==== begin registerFile(/WWW/pub2/data/ERD/person/376686/researchmap/presentations.jsonl) ====
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