『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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EID=374831EID:374831, Map:0, LastModified:2021年8月25日(水) 10:41:34, Operator:[三木 ちひろ], Avail:TRUE, Censor:0, Owner:[池田 康将], Read:継承, Write:継承, Delete:継承.
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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著者 (必須): 1.西村 賢二
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2. (英) Taguchi Kensei (日) (読)
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3.岸 誠司
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4. (英) Brooks Craig R (日) (読)
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5. (英) Ochi Arisa (日) (読)
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6. (英) Kadoya Hiroyuki (日) (読)
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7.池田 康将 ([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.生理系.薬理学]/[徳島大学.医学部.医学科.病態情報医学講座.薬理学分野]/[徳島大学.医科学教育部.医学専攻.病態情報医学講座]/[徳島大学.大学院医歯薬学研究部.医学域.医科学部門.生理系.薬理学])
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8. (英) Miyoshi Masashi (日) (読)
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9.田蒔 昌憲 ([徳島大学.病院.先端医科医療開発研究プロジェクト]/[徳島大学.病院.中央診療施設等.検査部]/[徳島大学.病院.診療科.内科.腎臓内科])
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10. (英) Abe Hideharu (日) (読)
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11. (英) Aihara Ken-Ichi (日) (読)
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12. (英) Kashihara Naoki (日) (読)
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13. (英) Nagai Kojiro (日) (読)
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題名 (必須): (英) Dual disruption of eNOS and ApoE gene accelerates kidney fibrosis and senescence after injury.  (日)    [継承]
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要約 (任意): (英) mice (DKO) were obtained by breeding. Unilateral ureteral obstruction (UUO) was performed on 8-10 week old male mice and the degree of renal tubular injury, fibrosis and kidney senescence were evaluated. DKO manifested elevated blood pressure, higher total cholesterol and lower HDL than WT. DKO showed sustained kidney injury molecule-1 protein expression. Kidney fibrosis was significantly higher in ApoEKO and DKO. mRNA expression of genes related to kidney fibrosis was the highest in DKO. The mRNA expression of Zinc-α2-Glycoprotein and heme oxygenase-1 were significantly decreased in DKO. Furthermore, mRNA expression of p53, p21 and p16 were increased both in ApoEKO and DKO, with DKO being the highest. Senescence associated β-gal positive tubule area was significantly increased in DKO. Increased DNA damage and target of rapamycin-autophagy spatial coupling compartments (TASCCs) formation was found in DKO. Mice with endothelial dysfunction and dyslipidemia developed kidney fibrosis and accelerated senescence even in young mice after injury. These data highlight the fact managing lifestyle-related diseases from a young age is important for CKD prevention.  (日)    [継承]
キーワード (推奨):
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誌名 (必須): Biochemical and Biophysical Research Communications ([Elsevier])
(pISSN: 0006-291X, eISSN: 1090-2104)

ISSN (任意): 1090-2104
ISSN: 0006-291X (pISSN: 0006-291X, eISSN: 1090-2104)
Title: Biochemical and biophysical research communications
Title(ISO): Biochem Biophys Res Commun
Publisher: Elsevier Inc.
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
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(必須): 142 148 [継承]
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年月日 (必須): 西暦 2021年 4月 9日 (令和 3年 4月 9日) [継承]
URL (任意):
DOI (任意): 10.1016/j.bbrc.2021.03.111    (→Scopusで検索) [継承]
PMID (任意): 33845306    (→Scopusで検索) [継承]
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備考 (任意): 1.(英) PublicationType: Journal Article  (日)    [継承]

標準的な表示

和文冊子 ● Kenji Nishimura, Kensei Taguchi, Seiji Kishi, R Craig Brooks, Arisa Ochi, Hiroyuki Kadoya, Yasumasa Ikeda, Masashi Miyoshi, Masanori Tamaki, Hideharu Abe, Ken-Ichi Aihara, Naoki Kashihara and Kojiro Nagai : Dual disruption of eNOS and ApoE gene accelerates kidney fibrosis and senescence after injury., Biochemical and Biophysical Research Communications, Vol.556, (号), 142-148, 2021.
欧文冊子 ● Kenji Nishimura, Kensei Taguchi, Seiji Kishi, R Craig Brooks, Arisa Ochi, Hiroyuki Kadoya, Yasumasa Ikeda, Masashi Miyoshi, Masanori Tamaki, Hideharu Abe, Ken-Ichi Aihara, Naoki Kashihara and Kojiro Nagai : Dual disruption of eNOS and ApoE gene accelerates kidney fibrosis and senescence after injury., Biochemical and Biophysical Research Communications, Vol.556, (号), 142-148, 2021.

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