Mallory-Denk body pathogenesis revisited

被引：32

作者：

French, Samuel W. ^{[1
]}

Bardag-Gorce, Fawzia ^{[1
]}

Li, Jun ^{[1
]}

French, Barbara A. ^{[1
]}

Oliva, Joan ^{[1
]}

机构：

[1] Harbor UCLA Med Ctr, Dept Pathol, 1000 W Carson St, Torrance, CA 90509 USA

来源：

WORLD JOURNAL OF HEPATOLOGY | 2010年 / 2卷 / 08期

关键词：

Toll-like receptor; Proinflammatory; Methyl donors; Epigenetic processes; Drug toxicity; 26s Protea-some; Immunoproteasome;

D O I：

10.4254/wjh.v2.i8.295

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

This editorial reviews the recent evidence showing that Mallory-Denk bodies (MDBs) form in hepatocytes as the result of a drug-induced shift from the 26s proteasome formation to the immunoproteasome formation. The shift is the result of changes in gene expression induced in promoter activation, which is induced by the IFN gamma and TNF alpha signaling pathway. This activates TLR 2 and 4 receptors. The TLR signaling pathway stimulates both the induction of a cytokine proinflammatory response and an up regulation of growth factors. The MDB- forming hepatocytes proliferate as a result of the increase in growth factor expression by the MDB-forming cells, which selectively proliferate in response to drug toxicity. All of these mechanisms are induced by drug toxicity, and are prevented by feeding the methyl donors SAMe and betaine, supporting the epigenetic response of MDB formation. (C) 2010 Baishideng. All rights reserved.

引用

页码：295 / 301

页数：7

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