Alcoholic liver disease and the gut-liver axis
Alcoholic liver disease and the gut-liver axis
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DOI：
10.3748/wjg.v16.i11.1321
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发表时间：
2010-03-21
影响因子：
4.3
通讯作者：
Bala, Shashi
中科院分区：
文献类型：
--
作者：
Szabo, Gyongyi;Bala, Shashi
酒精性肝病（ALD）是全球肝脏疾病和肝脏相关死亡的主要原因之一。在导致酒精性肝脏疾病发病的许多因素中，肠源性脂多糖（LPS）在诱导肝脏脂肪变性、炎症和纤维化方面发挥着核心作用。在这篇综述中，我们讨论了酒精有助于增加肠道通透性，库普弗细胞的激活，LPS的炎症级联反应的机制。Toll样受体4（TLR4）复合物在LPS识别中的作用以及TLR4诱导的信号传导途径在ALD中的重要性进行了评估。(C)2010年百世登。All rights reserved.
Alcoholic liver disease (ALD) is one of the leading causes of liver diseases and liver-related death worldwide. Of the many factors that contribute to the pathogenesis of ALD, gut-derived lipopolysaccharide (LPS) plays a central role in induction of steatosis, inflammation, and fibrosis in the liver. In this review, we discuss the mechanisms by which alcohol contributes to increased gut permeability, the activation of Kupffer cells, and the inflammatory cascade by LPS. The role of the Toll-like receptor 4 (TLR4) complex in LPS recognition and the importance of the TLR4-induced signaling pathways are evaluated in ALD. (C) 2010 Baishideng. All rights reserved.