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World J Gastroenterol. Mar 28, 2014; 20(12): 3078-3086
Published online Mar 28, 2014. doi: 10.3748/wjg.v20.i12.3078
Oxidative damage in the progression of chronic liver disease to hepatocellular carcinoma: An intricate pathway
Romilda Cardin, Marika Piciocchi, Marina Bortolami, Andromachi Kotsafti, Luisa Barzon, Enrico Lavezzo, Alessandro Sinigaglia, Kryssia Isabel Rodriguez-Castro, Massimo Rugge, Fabio Farinati
Romilda Cardin, Marika Piciocchi, Marina Bortolami, Andromachi Kotsafti, Kryssia Isabel Rodriguez-Castro, Fabio Farinati, Department of Surgery, Oncology and Gastroenterology, University of Padova, 35128 Padova, Italy
Luisa Barzon, Enrico Lavezzo, Alessandro Sinigaglia, Department of Molecular Medicine, University of Padova, 35128 Padova, Italy
Massimo Rugge, Department of Medicine, University of Padova, 35128 Padova, Italy
Author contributions: Cardin R, Piciocchi M, Bortolami M and Kotsafti A contributed to the conception, design and acquisition of data and approved the final version to be published; Barzon L, Lavezzo E and Sinigaglia A carried out the experiments related to miRNAs; Rodriguez-Castro KI revised the manuscript and approved the final version; Rugge M analyzed and interpreted the liver pathology; Farinati F proposed the study and drafted the manuscript.
Correspondence to: Fabio Farinati, MD, Professor, Department of Surgery, Oncology and Gastroenterology, University of Padova, Via Giustiniani 2, 35128 Padova, Italy. fabio.farinati@unipd.it
Telephone: +39-49-8211305 Fax: +39-49-8760820
Received: September 20, 2013
Revised: November 20, 2013
Accepted: January 6, 2014
Published online: March 28, 2014
Processing time: 187 Days and 19.4 Hours
Core Tip

Core tip: In this review, the relationship amongst chronic liver injury, free radical production, and development of hepatocellular carcinoma is explored. The review confirms the existence, in the intricate pathway involved in the progression of virus-related liver injury to cirrhosis and cancer, of a link between oxidative genomic and mitochondrial damage and telomere dysfunction. This link develops in the context of inflammatory response and induces a derangement of mechanisms controlling liver proliferation. In this scenario, mitochondria are emerging as a possible target for new treatments aimed at counteracting oxidative damage and disease progression to cancer, given their relevant role in inflammation and carcinogenesis.