Camps J, Joven J. Chemokine ligand 2 and paraoxonase-1 in non-alcoholic fatty liver disease: The search for alternative causative factors. World J Gastroenterol 2015; 21(10): 2875-2882 [PMID: 25780284 DOI: 10.3748/wjg.v21.i10.2875]
Corresponding Author of This Article
Jorge Joven, MD, PhD, Unitat de Recerca Biomèdica, Hospital Universitari de Sant Joan, Institut d’Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, c/ Sant Llorenç 21, 43201 Reus, Spain. jorge.joven@urv.cat
Research Domain of This Article
Biochemistry & Molecular Biology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Mar 14, 2015; 21(10): 2875-2882 Published online Mar 14, 2015. doi: 10.3748/wjg.v21.i10.2875
Chemokine ligand 2 and paraoxonase-1 in non-alcoholic fatty liver disease: The search for alternative causative factors
Jordi Camps, Jorge Joven
Jordi Camps, Jorge Joven, Unitat de Recerca Biomèdica, Hospital Universitari de Sant Joan, Institut d’Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, 43201 Reus, Spain
Author contributions: Both authors contributed equally to the interpretation and acquisition of data and the writing and approval of the manuscript.
Supported by Instituto de Salud Carlos III, No. PI08/1381, and No. PI11/00130; Carlos III Health Institute, Madrid, Spain; and the Fondo Europeo de Desarrollo Regional.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Jorge Joven, MD, PhD, Unitat de Recerca Biomèdica, Hospital Universitari de Sant Joan, Institut d’Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, c/ Sant Llorenç 21, 43201 Reus, Spain. jorge.joven@urv.cat
Telephone: +34-97-7310300 Fax: +34-97-759386
Received: July 14, 2014 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
Core Tip
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.
