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KAKEN_24790719seika.pdf
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Title |
Title |
肝臓線維化病態における、肝星細胞のFree cholesterol代謝機構の解明
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Kana |
カンゾウ センイカ ビョウタイ ニ オケル, カンセイ サイボウ ノ Free cholesterol タイシャ キコウ ノ カイメイ
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Kanzo senika byotai ni okeru, kansei saibo no Free cholesterol taisha kiko no kaimei
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Study on the mechanism of free cholesterol metabolism of hepatic stellate cell in liver fibrosis
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寺谷, 俊昭
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テラタニ, トシアキ
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Teratani, Toshiaki
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慶應義塾大学・医学部・助教
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Research team head
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科研費研究者番号 : 40624408
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2015
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科学研究費補助金研究成果報告書
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2014
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本邦では, メタボリックシンドロームの患者数増加に伴い, 非アルコール性脂肪肝炎の患者数が増大している。肝星細胞の遊離コレステロール蓄積は, TLR4シグナルの増大を介して, 肝星細胞のTGFβに対する感受性を増大させるが, 我々は細胞内コレステロール代謝関連遺伝子であるAcetyl-Coenzyme A acetyltransferase 1の欠損が, 肝臓線維化病態を増悪させることを明らかにした。Acetyl-Coenzyme A acetyltransferase 1は非アルコール性脂肪肝炎を含む肝臓線維化治療の有望な治療標的となるであろう。
Given the growing number of metabolic syndrome patients in recent years, the incidence of nonalcoholic steatohepatitis increases in Japan. Accumulation of free cholesterol in hepatic stellate cell (HSC) increased levels of Toll-like receptor 4 (TLR4), leading to down-regulation of bone morphogenetic protein and activin membrane-bound inhibitor (a pseudoreceptor for transforming growth factor [TGF]β); the HSCs became sensitized to TGFβ-induced activation. Acyl-coenzyme A: cholesterol acyltransferase (ACAT) catalyzes the conversion of free cholesterol to cholesterol ester, which prevents excess accumulation of free cholesterol. ACAT1 deficiency exaggerates liver fibrosis mainly through enhanced free cholesterol accumulation in HSCs. Regulation of ACAT1 activities in HSCs could be a target for treatment of liver fibrosis.
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研究種目 : 若手研究(B)
研究期間 : 2012~2014
課題番号 : 24790719
研究分野 : 消化器内科, 肝臓病学
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Jul 30, 2019 | | 著者,抄録 内容,言語 を変更 |
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