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Nmnat1 Deficiency Causes Mitoribosome Excess in Diabetic Nephropathy Mediated by Transcriptional Repressor HIC1
https://tokushima-u.repo.nii.ac.jp/records/2012210
https://tokushima-u.repo.nii.ac.jp/records/2012210f9d1bd8c-3b88-43ef-933a-3680096e67e1
| 名前 / ファイル | ライセンス | アクション |
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ijms_25_12_6384.pdf (17 MB)
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| Item type | 文献 / Documents(1) | |||||||||||||||||||||||||||||
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| 公開日 | 2024-08-16 | |||||||||||||||||||||||||||||
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| アクセス権 | open access | |||||||||||||||||||||||||||||
| 資源タイプ | ||||||||||||||||||||||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||||||||||||||||||||||
| 資源タイプ | journal article | |||||||||||||||||||||||||||||
| 出版社版DOI | ||||||||||||||||||||||||||||||
| 関連識別子 | https://doi.org/10.3390/ijms25126384 | |||||||||||||||||||||||||||||
| 関連名称 | 10.3390/ijms25126384 | |||||||||||||||||||||||||||||
| 出版タイプ | ||||||||||||||||||||||||||||||
| 出版タイプ | VoR | |||||||||||||||||||||||||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||||||||||||||||||||||
| タイトル | ||||||||||||||||||||||||||||||
| タイトル | Nmnat1 Deficiency Causes Mitoribosome Excess in Diabetic Nephropathy Mediated by Transcriptional Repressor HIC1 | |||||||||||||||||||||||||||||
| 著者 |
長谷川, 一宏
× 長谷川, 一宏
WEKO
1450
× 田蒔, 昌憲
WEKO
905
× サカマキ, ユウスケ
× 𦚰野, 修
WEKO
1429
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| 内容記述 | Nicotinamide adenine dinucleotide (NAD) is involved in renal physiology and is synthesized by nicotinamide mononucleotide adenylyltransferase (NMNAT). NMNAT exists as three isoforms, namely, NMNAT1, NMNAT2, and NMNAT3, encoded by Nmnat1, Nmnat2, and Nmnat3, respectively. In diabetic nephropathy (DN), NAD levels decrease, aggravating renal fibrosis. Conversely, sodium–glucose cotransporter-2 inhibitors increase NAD levels, mitigating renal fibrosis. In this regard, renal NAD synthesis has recently gained attention. However, the renal role of Nmnat in DN remains uncertain. Therefore, we investigated the role of Nmnat by establishing genetically engineered mice. Among the three isoforms, NMNAT1 levels were markedly reduced in the proximal tubules (PTs) of db/db mice. We examined the phenotypic changes in PT-specific Nmnat1 conditional knockout (CKO) mice. In CKO mice, Nmnat1 expression in PTs was downregulated when the tubules exhibited albuminuria, peritubular type IV collagen deposition, and mitochondrial ribosome (mitoribosome) excess. In CKO mice, Nmnat1 deficiency-induced mitoribosome excess hindered mitoribosomal translation of mitochondrial inner membrane-associated oxidative phosphorylation complex I (CI), CIII, CIV, and CV proteins and mitoribosomal dysfunction. Furthermore, the expression of hypermethylated in cancer 1, a transcription repressor, was downregulated in CKO mice, causing mitoribosome excess. Nmnat1 overexpression preserved mitoribosomal function, suggesting its protective role in DN. | |||||||||||||||||||||||||||||
| キーワード | ||||||||||||||||||||||||||||||
| 主題 | Nmnat1 | |||||||||||||||||||||||||||||
| キーワード | ||||||||||||||||||||||||||||||
| 主題 | mitoribosome | |||||||||||||||||||||||||||||
| キーワード | ||||||||||||||||||||||||||||||
| 主題 | diabetic nephropathy | |||||||||||||||||||||||||||||
| 書誌情報 |
en : International Journal of Molecular Sciences 巻 25, 号 12, p. 6384, 発行日 2024-06-09 |
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| 収録物識別子タイプ | ISSN | |||||||||||||||||||||||||||||
| 収録物識別子 | 14220067 | |||||||||||||||||||||||||||||
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| 出版者 | MDPI | |||||||||||||||||||||||||||||
| 権利情報 | ||||||||||||||||||||||||||||||
| 権利情報 | This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). | |||||||||||||||||||||||||||||
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| 識別子 | 410124 | |||||||||||||||||||||||||||||
| 言語 | ||||||||||||||||||||||||||||||
| 言語 | eng | |||||||||||||||||||||||||||||
