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  1. 川崎医学会機関誌
  2. Kawasaki Medical Journal
  3. Vol.49(2023)

The deficient of eNOS-NO pathway exacerbates kidney dysfunction via inflammasome activation in diabetic kidney disease

https://kwmed.repo.nii.ac.jp/records/2000068
https://kwmed.repo.nii.ac.jp/records/2000068
056afe7e-c6cd-49ad-a475-ec6741ae0fc9
名前 / ファイル ライセンス アクション
KMJ-E202349047.pdf PDF
Item type 学術雑誌論文 / Journal Article(1)
公開日 2024-06-26
タイトル
タイトル The deficient of eNOS-NO pathway exacerbates kidney dysfunction via inflammasome activation in diabetic kidney disease
言語 en
言語
言語 eng
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
著者 UMENO, Reina

× UMENO, Reina

en UMENO, Reina

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NAGASU, Hajime

× NAGASU, Hajime

en NAGASU, Hajime

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TAKASU, Masanobu

× TAKASU, Masanobu

en TAKASU, Masanobu

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INOUE, Natsumi

× INOUE, Natsumi

en INOUE, Natsumi

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TATSUGAWA, Rie

× TATSUGAWA, Rie

en TATSUGAWA, Rie

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KAJIMOTO, Eriko

× KAJIMOTO, Eriko

en KAJIMOTO, Eriko

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HIRANO, Tomoko

× HIRANO, Tomoko

en HIRANO, Tomoko

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IWAKURA, Tsukasa

× IWAKURA, Tsukasa

en IWAKURA, Tsukasa

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WADA, Yoshihisa

× WADA, Yoshihisa

en WADA, Yoshihisa

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KADOYA, Hiroyuki

× KADOYA, Hiroyuki

en KADOYA, Hiroyuki

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KIDOKORO, Kengo

× KIDOKORO, Kengo

en KIDOKORO, Kengo

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KISHI, Seiji

× KISHI, Seiji

en KISHI, Seiji

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TANIGUCHI, Shun’ichiro

× TANIGUCHI, Shun’ichiro

en TANIGUCHI, Shun’ichiro

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TAKAHASHI, Masafumi

× TAKAHASHI, Masafumi

en TAKAHASHI, Masafumi

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SASAKI, Tamaki

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en SASAKI, Tamaki

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KASHIHARA, Naoki

× KASHIHARA, Naoki

en KASHIHARA, Naoki

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著者所属(英)
言語 en
値 Departments of Nephrology and Hypertension
著者所属(英)
言語 en
値 Departments of Nephrology and Hypertension
著者所属(英)
言語 en
値 Departments of Nephrology and Hypertension
著者所属(英)
言語 en
値 Departments of Nephrology and Hypertension
著者所属(英)
言語 en
値 Departments of Nephrology and Hypertension
著者所属(英)
言語 en
値 Departments of Nephrology and Hypertension
著者所属(英)
言語 en
値 Departments of Nephrology and Hypertension
著者所属(英)
言語 en
値 Departments of Nephrology and Hypertension
著者所属(英)
言語 en
値 Departments of Nephrology and Hypertension
著者所属(英)
言語 en
値 Departments of General Geriatric Medicine, Kawasaki Medical School
著者所属(英)
言語 en
値 Departments of Nephrology and Hypertension
著者所属(英)
言語 en
値 Departments of Nephrology and Hypertension
著者所属(英)
言語 en
値 Advanced Cancer Medicine for Gynecologic Cancer, Kagoshima University Graduate School of Medical and Dental Sciences
著者所属(英)
言語 en
値 Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University
著者所属(英)
言語 en
値 Departments of Nephrology and Hypertension
著者所属(英)
言語 en
値 Faculty of Medicine, Kawasaki Medical School
キーワード
言語 en
主題Scheme Other
主題 Endothelial cell
キーワード
言語 en
主題Scheme Other
主題 ASC-deficient mice
キーワード
言語 en
主題Scheme Other
主題 Chronic inflammation
キーワード
言語 en
主題Scheme Other
主題 Diabetes mellitus
抄録(英)
言語 en
値 Background: Diabetic kidney disease (DKD) is a major cause of end-stage kidney disease. We have reported that inflammasome activation is involved in the pathogenesis of kidney disease and that the disruption of the endothelial nitric oxide synthase (eNOS)- nitric oxide (NO) pathway promotes inflammasome activation and renal interstitial inflammation in hypertensive and aging kidney models. Endothelial dysfunction, which is involved in the pathogenesis of renal injury, may regulate inflammasome activation. However, it is not known whether endothelial dysfunction promotes the progression of DKD via inflammasome activation.<br>Methods: Apoptosis-associated speck-like protein (ASC) is one of the components constituting the inflammasome. We crossed eNOS-deficient mice (eNOSKO) with ASC-deficient mice to create eNOS-ASC-double-deficient mice (eNOS-ASC-DKO). C57BL / 6 (WT), eNOSKO and eNOS-ASC-DKO were administered streptozotocin (STZ) to induce diabetes. Urine storage and blood pressure measurements were taken in these groups. Eight weeks after the onset of diabetes, they were sacrificed and examined. Tissue damage was examined by PAS staining, Masson staining, and tissue immunohistochemistry.<br>Results: The exacerbation of glomerular lesions were observed in eNOSKO-STZ mice. Kidney injury molecule-1 (KIM-1) positive impaired proximal tubules increased as well. The interstitial fibrosis was significantly increased. These changes were rescued by ASC deficiency. In addition, macrophage infiltrated into the glomeruli in eNOS-deficient mice. Interestingly, these inflammatory cell infiltrations were suppressed in eNOS-ASC-DKO-STZ mice.<br>Conclusions: This study used a DKD model to demonstrate the impact of endothelial dysfunction on chronic inflammation. The results indicate that controlling inflammasome activation may inhibit the progression of kidney disease.
書誌情報 en : Kawasaki medical journal

巻 49, p. 47-55, 発行日 2023
出版者
出版者 Kawasaki Medical Society
言語 en
ISSN
収録物識別子タイプ EISSN
収録物識別子 24343404
書誌レコードID
収録物識別子タイプ NCID
収録物識別子 AA12029005
DOI
関連タイプ isIdenticalTo
識別子タイプ DOI
関連識別子 https://doi.org/10.11482/KMJ-E202349047
記事種別(英)
内容記述 Regular Article
言語 en
関連サイト
識別子タイプ URI
関連識別子 https://igakkai.kms-igakkai.com/wp/wp-content/uploads/2023en/KMJ-E202349047.pdf
著者版フラグ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
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