Disease-specific mechanisms of fibrosis: hepatitis C virus and nonalcoholic steatohepatitis.
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.
van der Poorten
David
D
Storr Liver Unit, Westmead Millennium Institute, Westmead NSW, Australia.
George
Jacob
J
D054392:Adipokines / Q000378:metabolism; D000818:Animals; D017209:Apoptosis; D005234:Fatty Liver / Q000276:immunology / Q000821:virology*; D016174:Hepacivirus / Q000502:physiology; D055166:Hepatic Stellate Cells / Q000276:immunology / Q000821:virology*; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000276:immunology; D006801:Humans; D007333:Insulin Resistance; D050356:Lipid Metabolism; D008103:Liver Cirrhosis / Q000276:immunology / Q000821:virology*; D018384:Oxidative Stress; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology
D054392:Adipokines