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World J Gastroenterol. Oct 21, 2014; 20(39): 14205-14218
Published online Oct 21, 2014. doi: 10.3748/wjg.v20.i39.14205
Oxidative stress, cardiolipin and mitochondrial dysfunction in nonalcoholic fatty liver disease
Giuseppe Paradies, Valeria Paradies, Francesca M Ruggiero, Giuseppe Petrosillo
Giuseppe Paradies, Valeria Paradies, Francesca M Ruggiero, Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, 70126 Bari, Italy
Giuseppe Petrosillo, Institute of Biomembranes and Bioenergetics, National Research Council, 70126 Bari, Italy
Author contributions: Paradies G, Paradies V, Ruggiero FM and Petrosillo G contributed to the manuscript.
Correspondence to: Giuseppe Paradies, Professor, Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, via E Orabona 4, 70126 Bari, Italy. g.paradies@biologia.uniba.it
Telephone: +39-80-5443324  Fax: +39-80-5443317
Received: November 19, 2013
Revised: February 13, 2014
Accepted: June 26, 2014
Published online: October 21, 2014
Processing time: 334 Days and 22.3 Hours
Core Tip

Core tip: Nonalcoholic fatty liver disease (NAFLD) is considered the most common form of chronic liver disease. Mitochondrial dysfunction and oxidative stress play a key role in the physiopathology of NAFLD. Mitochondrial respiratory chain is the main source of reactive oxygen species, which may damage mitochondrial proteins, lipids and mitochondrial DNA. Cardiolipin, a phospholipid of the inner mitochondrial membrane, plays an important role in mitochondrial bioenergetics and in apoptosis. Cardiolipin abnormalities have been associated with mitochondrial dysfunction in several physiopathological conditions, including NAFLD. In this review, we focus on the potential roles played by oxidative stress and cardiolipin alterations in mitochondrial dysfunction in NAFLD.