『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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種別 (必須): 学術論文 (審査論文) [継承]
言語 (必須): 英語 [継承]
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カテゴリ (推奨):
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学究種別 (推奨):
組織 (推奨):
著者 (必須): 1. (英) Ida-Naitoh Makiko (日) (読)
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2. (英) Tokuyama Hirobumi (日) (読)
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3. (英) Futatsugi Koji (日) (読)
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4. (英) Yasuda Marie (日) (読)
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5. (英) Adachi Keika (日) (読)
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6. (英) Kanda Takeshi (日) (読)
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7. (英) Tanabe Yoshiyuki (日) (読)
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8.𦚰野 修 ([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.内科系.腎臓内科学])
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9. (英) Itoh Hiroshi (日) (読)
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題名 (必須): (英) Proximal-tubule molecular relay from early Protein diaphanous homolog 1 to late Rho-associated protein kinase 1 regulates kidney function in obesity-induced kidney damage.  (日)    [継承]
副題 (任意):
要約 (任意): (英) The small GTPase protein RhoA has two effectors, ROCK (Rho-associated protein kinase 1) and mDIA1 (protein diaphanous homolog 1), which cooperate reciprocally. However, temporal regulation of RhoA and its effectors in obesity-induced kidney damage remains unclear. Here, we investigated the role of RhoA activation in the proximal tubules at the early and late stages of obesity-induced kidney damage. In mice, a three-week high-fat-diet induced proximal tubule hypertrophy and damage without increased albuminuria, and RhoA/mDIA1 activation without ROCK activation. Conversely, a 12-week high-fat diet induced proximal tubule hypertrophy, proximal tubule damage, increased albuminuria, and RhoA/ROCK activation without mDIA1 elevation. Proximal tubule hypertrophy resulting from cell cycle arrest accompanied by downregulation of the multifunctional cyclin-dependent kinase inhibitor p27Kip1 was elicited by RhoA activation. Mice overexpressing proximal tubule-specific and dominant-negative RHOA display amelioration of high-fat diet-induced kidney hypertrophy, cell cycle abnormalities, inflammation, and renal impairment. In human proximal tubule cells, mechanical stretch mimicking hypertrophy activated ROCK, which triggered inflammation. In human kidney samples from normal individuals with a body mass index of about 25, proximal tubule cell size correlated with body mass index, proximal tubule cell damages, and mDIA1 expression. Thus, RhoA activation in proximal tubules is critical for the initiation and progression of obesity-induced kidney damage. Hence, the switch in the downstream RhoA effector in proximal tubule represents a transition from normal to pathogenic kidney adaptation and to body weight gain, leading to obesity-induced kidney damage.  (日)    [継承]
キーワード (推奨): 1. (英) Albuminuria (日) (読) [継承]
2. (英) Animals (日) (読) [継承]
3. (英) Cyclin-Dependent Kinases (日) (読) [継承]
4. (英) Humans (日) (読) [継承]
5. (英) Hypertrophy (日) (読) [継承]
6. (英) Inflammation (日) (読) [継承]
7. (英) Kidney Tubules, Proximal (日) (読) [継承]
8. (英) Mice (日) (読) [継承]
9. (英) Obesity (日) (読) [継承]
10. (英) rho-Associated Kinases (日) (読) [継承]
発行所 (推奨):
誌名 (必須): Kidney International ([The International Society of Nephrology])
(pISSN: 0085-2538, eISSN: 1523-1755)

ISSN (任意): 1523-1755
ISSN: 0085-2538 (pISSN: 0085-2538, eISSN: 1523-1755)
Title: Kidney international
Title(ISO): Kidney Int
Publisher: Elsevier B.V.
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
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年月日 (必須): 西暦 2022年 6月 15日 (令和 4年 6月 15日) [継承]
URL (任意):
DOI (任意): 10.1016/j.kint.2022.05.018    (→Scopusで検索) [継承]
PMID (任意): 35716954    (→Scopusで検索) [継承]
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備考 (任意): 1.(英) PublicationType: Journal Article  (日)    [継承]
2.(英) PublicationType: Research Support, Non-U.S. Gov't  (日)    [継承]

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和文冊子 ● Makiko Ida-Naitoh, Hirobumi Tokuyama, Koji Futatsugi, Marie Yasuda, Keika Adachi, Takeshi Kanda, Yoshiyuki Tanabe, Shu Wakino and Hiroshi Itoh : Proximal-tubule molecular relay from early Protein diaphanous homolog 1 to late Rho-associated protein kinase 1 regulates kidney function in obesity-induced kidney damage., Kidney International, 102, 4, 798-814, 2022.
欧文冊子 ● Makiko Ida-Naitoh, Hirobumi Tokuyama, Koji Futatsugi, Marie Yasuda, Keika Adachi, Takeshi Kanda, Yoshiyuki Tanabe, Shu Wakino and Hiroshi Itoh : Proximal-tubule molecular relay from early Protein diaphanous homolog 1 to late Rho-associated protein kinase 1 regulates kidney function in obesity-induced kidney damage., Kidney International, 102, 4, 798-814, 2022.

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