库普弗电池
发病机制
酒精性肝病
肝病
细胞因子
NADPH氧化酶
基因剔除小鼠
肝损伤
基因敲除
化学
细胞生物学
免疫学
生物
生物化学
医学
基因
氧化应激
药理学
内科学
肝硬化
作者
Michael D. Wheeler,Hiroshi Kono,Ming Yin,Mikio Nakagami,Takehiko Uesugi,Gavin E. Arteel,Erwin Gábele,Ivan Rusyn,Shunhei Yamashina,Matthias Froh,Yuki Adachi,Yuji Iimuro,Blair U. Bradford,Olivia M. Smutney,Henry D. Connor,Ronald P. Mason,Sanna M. Goyert,Jeff M. Peters,Frank J. Gonzalez,R. Jude Samulski,Ronald G. Thurman
标识
DOI:10.1016/s0891-5849(01)00748-1
摘要
Considerable evidence for a role of Kupffer cells in alcoholic liver disease has accumulated and they have recently been shown to be a predominant source of free radicals. Several approaches including pharmacological agents, knockout mice, and viral gene transfer have been used to fill critical gaps in understanding key mechanisms by which Kupffer cell activation, oxidant formation, and cytokine production lead to liver damage and subsequent pathogenesis. This review highlights new data in support of the hypothesis that Kupffer cells play a pivotal role in hepatotoxicity due to ethanol by producing oxidants via NADPH oxidase.
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