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©2007 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Sep 21, 2007; 13(35): 4746-4754
Published online Sep 21, 2007. doi: 10.3748/wjg.v13.i35.4746
Published online Sep 21, 2007. doi: 10.3748/wjg.v13.i35.4746
Role of iron in hepatic fibrosis: One piece in the puzzle
Marie A Philippe, Richard G Ruddell, Grant A Ramm, Hepatic Fibrosis Group, The Queensland Institute of Medical Research, PO Royal Brisbane and Women’s Hospital, Brisbane 4029, Australia
Author contributions: All authors contributed equally to the work.
Supported by NHMRC Program Grant 339400
Correspondence to: Grant A Ramm, PhD, Associate Professor, Hepatic Fibrosis Group, The Queensland Institute of Medical Research, PO Royal Brisbane and Women’s Hospital, Brisbane 4029, Australia. grant.ramm@qimr.edu.au
Telephone: +61-7-33620177 Fax: +61-7-33620108
Received: March 27, 2007
Revised: April 10, 2007
Accepted: April 17, 2007
Published online: September 21, 2007
Revised: April 10, 2007
Accepted: April 17, 2007
Published online: September 21, 2007
Abstract
Iron is an essential element involved in various biological pathways. When present in excess within the cell, iron can be toxic due to its ability to catalyse the formation of damaging radicals, which promote cellular injury and cell death. Within the liver, iron related oxidative stress can lead to fibrosis and ultimately to cirrhosis. Here we review the role of excessive iron in the pathologies associated with various chronic diseases of the liver. We also describe the molecular mechanism by which iron contributes to the development of hepatic fibrosis.
Keywords: Iron, Fibrosis, Oxidative stress, Hepatic stellate cell, Haemochromatosis, Hepatitis C, Non-alcoholic fatty liver disease, Alcoholic liver disease