©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Mar 7, 2017; 23(9): 1513-1520
Published online Mar 7, 2017. doi: 10.3748/wjg.v23.i9.1513
Published online Mar 7, 2017. doi: 10.3748/wjg.v23.i9.1513
P-glycoprotein multidrug transporter in inflammatory bowel diseases: More questions than answers
Elke Cario, Experimental Gastroenterology, Department of Gastroenterology and Hepatology, University Hospital Essen, Medical School, University of Duisburg-Essen, 45147 Essen, Germany
Author contributions: Cario E contributed all to this manuscript.
Supported by the Deutsche Forschungsgemeinschaft , No. CA226/4-3 to Cario E .
Conflict-of-interest statement: Cario E declares no conflict of interest related to this publication.
Correspondence to: Elke Cario, MD, Professor, Experimental Gastroenterology, Department of Gastroenterology and Hepatology, University Hospital Essen, Medical School, University of Duisburg-Essen, Hufelandstr. 55, D-45122 Essen, 45147 Essen, Germany. elke.cario@uni-due.de
Telephone: +49-201-7234527 Fax: +49-201-7236858
Received: November 24, 2016
Peer-review started: November 27, 2016
First decision: December 19, 2016
Revised: January 6, 2017
Accepted: February 16, 2017
Article in press: February 17, 2017
Published online: March 7, 2017
Processing time: 101 Days and 17.6 Hours
Peer-review started: November 27, 2016
First decision: December 19, 2016
Revised: January 6, 2017
Accepted: February 16, 2017
Article in press: February 17, 2017
Published online: March 7, 2017
Processing time: 101 Days and 17.6 Hours
Core Tip
Core tip: Altered levels of p-glycoprotein (p-gp) expression as well as genetic variants of ABCB1/MDR1 have been associated with inflammatory bowel diseases (IBD). Decreased efflux activity of p-gp may promote disease susceptibility, while increased efflux activity may impair drug responses in IBD. In this Editorial, I highlight what we need to know about this transporter and xenobiotic signaling pathways in order to better understand its potential pathophysiology in IBD and develop targeted therapies.