Published online Mar 14, 2015. doi: 10.3748/wjg.v21.i10.2875
Peer-review started: July 15, 2014
First decision: August 15, 2014
Revised: September 2, 2014
Accepted: September 29, 2014
Article in press: September 30, 2014
Published online: March 14, 2015
Processing time: 244 Days and 21.3 Hours
Core tip: Recently acquired knowledge on the role of oxidation, inflammation and mitochondrial dysfunction in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) suggests a crucial role in the search for biological markers and therapeutic targets to alleviate the progression of the disease. Classically associated with obesity, the pathogenesis of NAFLD is extremely complex and mostly unknown. Consequently, the correct clinical management and prevention has not been established yet. Despite disparate results in the literature, mainly due to the different methods to measure the oxidative stress, there is currently no doubt that oxidative stress plays a crucial role. Similarly, the infiltration of monocytes, mainly due to the action of chemokines, is a relevant factor. However, to uncover the actual molecular mechanisms has proven to be more difficult than expected. The role of both oxidation and inflammation could be considered defensive and/or causative but the combination of these and other mechanisms may improve the understanding of NAFLD as a manifestation of mitochondrial disease. J. Camps and J. Joven. Chemokine ligand 2 and paraoxonase-1 in non-alcoholic fatty liver disease: the search for alternative causative factors.