Disease-Specific Mechanisms of Fibrosis: Hepatitis C Virus and Nonalcoholic Steatohepatitis

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• 作者：David van der Poorten ; BSc (med) MBBS^a ; ^b ; Jacob George ; MBBS ; PhD^a ; ^b ; ^{j.george@usyd.edu.au}
• 关键词：Fibrosis ; Hepatitis C ; Nonalcoholic steatohepatitis ; Nonalcoholic fatty liver disease ; Pathogenesis ; Insulin resistance
• 刊名：Clinics in Liver Disease
• 出版年：2008
• 出版时间：November 2008
• 年：2008
• 卷：12
• 期：4
• 页码：805-824
• 全文大小：308 K

文摘

Our mechanistic understanding of liver fibrosis has increased dramatically in recent years for all liver diseases and for hepatitis C and nonalcoholic steatohepatitis (NASH) in particular. Hepatitis C causes liver injury and fibrosis through direct cytopathic means, direct and indirect interactions with hepatic stellate cells, and activation of the immune system. Steatosis and insulin resistance, which are intrinsic deficits in NASH, are also of great importance in hepatitis C and may be induced by viral or host metabolic factors. For NASH, the key mediators of damage include oxidative stress, fat compartmentalization, visceral fat, apoptosis, and adipokine derangement. This article explores in depth the disease-specific mechanisms of fibrosis in hepatitis C and NASH, with a focus on recent developments.