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      저자 : ( Vishnudutt Purohit ) (검색결과 1 건)
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      • Alcohol and Liver Molecular Pathogenesis In Alcoholic Liver Disease -Inflammation, Fibrosis, And Cancer

        ( Vishnudutt Purohit ),( Bin Gao ) 대한소화기학회 2007 SIDDS Vol.9 No.-

        This review summarizes the mechanisms of alcoholic liver inflammation, fibrosis, and hepatocellular carcinoma (HCC), which are progressive stages of alcoholic liver disease. Chronic alcohol consumption may lead to the development of liver inflammation through a cascade of events that include increased transfer of endotoxin from intestine to the liver; endotoxin-induced Kupffer cell activation through oxidative stress and NF-kB/Egr-1 activation; production of TNF-α, chemokines, and adhesion molecules; sensitization of hepatocytes to inflammatory mediators; and recruitment of inflammatory cells. Various factors such as acetaldehyde, oxidative stress, TGF-β, and hepatocyte apoptotic bodies may contribute to the activation of hepatic stellate cells, which may result in increased collagen deposition contributing to liver fibrosis. The major intracellular signal transduction pathways involved in collagen production are PKC, MAPK (p38, JNK, and ERK1/2) and PI3K. The major transcription factors for collagen transcription are C/EBP-β, Sp1, Smad 3, and Smad 4. Alcohol may also promote liver fibrosis by modulating innate immune system via promoting pro-fibrotic effects of Kupffer cells and suppressing anti-fibrotic effects of NK cells. Chronic alcohol exposure may initiate and/or promote the development of HCC by excess accumulation of acetaldehyde, which in turn may form DNA adducts and induce mutations. Free radicals, especially hydroxyl radicals and lipid peroxidation products, generated in response to ethanol exposure may also contribute to DNA adduct formation and mutations. Finally, abnormal DNA methylation caused by ethanol-induced s-adenosylmethionine deficiency may also trigger malignant transformation.

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