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Oxidative damage in the progression of chronic liver disease to hepatocellular carcinoma:An intricate pathway

World Journal of Gastroenterology 2014年第12期20卷 3078-3086页

作者： Romilda Cardin Marika Piciocchi Marina Bortolami Andromachi Kotsafti luisa barzon Enrico Lavezzo Alessandro Sinigaglia Kryssia Isabel Rodriguez-Castro Massimo Rugge Fabio Farinati Department of Surgery Oncology and GastroenterologyUniversity of Padova Department of Molecular Medicine University of Padova Department of Medicine University of Padova

The histo-pathologic and molecular mechanisms leading to initiation and progression of hepatocellular carcinoma (HCC) are still ill-defined; however, there is increasing evidence that the gradual accumulation of mutations, genetic and epigenetic changes which occur in preneoplastic hepatocytes results in the development of dysplastic foci, nodules, and finally, overt HCC. As well as many other neoplasias, liver cancer is considered an “inflammatory cancer”, arising from a context of inflammation, and characterized by inflammation-related mechanisms that favor tumor cell survival, proliferation, and invasion. Molecular mechanisms that link inflammation and neoplasia have been widely investigated, and it has been well established that inflammatory cells recruited at these sites with ongoing inflammatory activity release chemokines that enhance the production of reactive oxygen species. The latter, in turn, probably have a major pathogenic role in the continuum starting from hepatitis followed by chronic inflammation, and ultimately leading to cancer. The relationship amongst chronic liver injury, free radical production, and development of HCC is explored in the present review, particularly in the light of the complex network that involves oxidative DNA damage, cytokine synthesis, telomere dysfunction, and microRNA regulation.

关键词： Reactive oxygen species Viral hepatitis Hepatocellular carcinoma Telomere dysfunction Cytokines mitochondria Antioxidant mechanisms MicroRNA and circulating free DNA

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