Hepatic tight junctions: From viral entry to cancer metastasis

被引:26
作者
Lee, Nikki P. [3 ]
Luk, John M. [1 ,2 ]
机构
[1] Natl Univ Singapore, Dept Pharmacol, Natl Univ Hlth Syst, Singapore 117597, Singapore
[2] Natl Univ Singapore, Dept Surg, Natl Univ Hlth Syst, Singapore 117597, Singapore
[3] Queen Mary Hosp, Dept Surg, Hong Kong, Hong Kong, Peoples R China
关键词
Tight junctions; Hepatocytes; Blood-biliary barrier; Bile canaliculi; Hepatitis; Liver steatosis; Liver neoplasms; C VIRUS ENTRY; HEPATOCELLULAR-CARCINOMA; SIGNALING PATHWAYS; COLORECTAL-CANCER; DIFFERENTIAL EXPRESSION; SEMINIFEROUS EPITHELIUM; CLAUDIN-1; EXPRESSION; MOLECULAR-MECHANISMS; ADENOVIRUS-RECEPTOR; TUMOR ANGIOGENESIS;
D O I
10.3748/wjg.v16.i3.289
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
The tight junction (TJ) is a critical cellular component for maintenance of tissue integrity, cellular interactions and cell-cell communications, and physiologically functions as the "great wall" against external agents and the surrounding hostile environment. During the host-pathogen evolution, viruses somehow found the key to unlock the gate for their entry into cells and to exploit and exhaust the host cells. In the liver, an array of TJ molecules is localized along the bile canaliculi forming the blood-biliary barrier, where they play pivotal roles in paracellular permeability, bile secretion, and cell polarity. In pathology, certain hepatic TJ molecules mediate virus entry causing hepatitis infection; deregulation and functional abnormality of the TJ have also been implicated in triggering liver cancer development and metastasis. All these findings shed new insights on the understanding of hepatic TJs in the development of liver disease and provide new clues for potential intervention. (C) 2010 Baishideng. All rights reserved.
引用
收藏
页码:289 / 295
页数:7
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