Martín-Sanz P, Casado M, Boscá L. Cyclooxygenase 2 in liver dysfunction and carcinogenesis: Facts and perspectives. World J Gastroenterol 2017; 23(20): 3572-3580 [PMID: 28611510 DOI: 10.3748/wjg.v23.i20.3572]
Corresponding Author of This Article
Lisardo Boscá, PhD, Department of Metabolism and Cell Signaling, Institute of Biomedical Research Alberto Sols, Arturo Duperier 4, Madrid 28029, Spain. lbosca@iib.uam.es
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Editorial
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. May 28, 2017; 23(20): 3572-3580 Published online May 28, 2017. doi: 10.3748/wjg.v23.i20.3572
Cyclooxygenase 2 in liver dysfunction and carcinogenesis: Facts and perspectives
Paloma Martín-Sanz, Marta Casado, Lisardo Boscá
Paloma Martín-Sanz, Lisardo Boscá, Department of Metabolism and Cell Signaling, Institute of Biomedical Research Alberto Sols, Madrid 28029, Spain
Paloma Martín-Sanz, Marta Casado, Lisardo Boscá, Biomedical Network Center for the Study of Hepatic and Digestive Disease, and Cardiovascular Diseases, Madrid 28029, Spain
Marta Casado, Metabolic Experimental Pathology Unit, Biomedical Institute of Valencia, Jaume Roig 11, Valencia 46010, Spain
Author contributions: Martín-Sanz P and Casado M contributed with the development of experimental models; Boscá L discussed the data; Martín-Sanz P, Casado M and Boscá L revised the literature and conceived the issues which formed the content of the manuscript.
Supported byMINECO, Spain, No. SAF2014-52492R; COOPB20213 (CSIC), No. SAF2013-43713R and No. SAF2016-75004R; ISCIII, Spain, CIBERcv and CIBERehd; We thank FEDER for financial support.
Conflict-of-interest statement: The authors declare no conflict of interests.
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: Lisardo Boscá, PhD, Department of Metabolism and Cell Signaling, Institute of Biomedical Research Alberto Sols, Arturo Duperier 4, Madrid 28029, Spain. lbosca@iib.uam.es
Telephone: +34-914-972747 Fax: +34-914-972746
Received: January 25, 2017 Peer-review started: February 1, 2017 First decision: February 23, 2017 Revised: March 3, 2017 Accepted: April 12, 2017 Article in press: April 12, 2017 Published online: May 28, 2017 Processing time: 121 Days and 23.1 Hours
Abstract
The biosynthesis of prostaglandins and thromboxanes has been a focus of interest in the management of many liver diseases. Cyclooxygenases are the enzymes involved in the first step of the biosynthesis of these lipid mediators and selective inhibitors for these isoenzymes as well as pharmacological analogues of prostaglandins have been developed and are currently applied therapeutically. Here we discuss the implications of these enzymes in the onset of metabolic and lipid disorders in the liver and their potential role in the progression of the diseases towards fibrosis and hepatocellular carcinogenesis.
Core tip: The assessment of the role of Cyclooxygenase-2 (COX-2) in hepatic diseases, ranging from non-alcoholic steatohepatitis to hepatocellular carcinoma, constitutes a field in which controversy exists probably because of the use of different experimental models. Since potent and selective inhibitors of COX-2 exist, but also stable PGE2 analogues to be used in therapy, unraveling the precise contribution of this enzyme and its products to the prevention of the progress of liver dysfunctions appears to be a useful approach for managing liver diseases.
