Samant H, Manatsathit W, Dies D, Shokouh-Amiri H, Zibari G, Boktor M, Alexander JS. Cholestatic liver diseases: An era of emerging therapies. World J Clin Cases 2019; 7(13): 1571-1581 [PMID: 31367616 DOI: 10.12998/wjcc.v7.i13.1571]
Corresponding Author of This Article
Jonathan Steve Alexander, FACG, PhD, Professor, Department of Molecular and Cellular Physiology, Louisiana State University, School of Medicine, 1501 Kings Highway, Shreveport, LA 71103, United States. jalexa@lsuhsc.edu
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Minireviews
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 Clin Cases. Jul 6, 2019; 7(13): 1571-1581 Published online Jul 6, 2019. doi: 10.12998/wjcc.v7.i13.1571
Cholestatic liver diseases: An era of emerging therapies
Hrishikesh Samant, Wuttiporn Manatsathit, David Dies, Hosein Shokouh-Amiri, Gazi Zibari, Moheb Boktor, Jonathan Steve Alexander
Hrishikesh Samant, Moheb Boktor, Division of Gastroenterology and Hepatology, Department of medicine, LSU health, Shreveport, LA 71103, United States
Hrishikesh Samant, David Dies, Hosein Shokouh-Amiri, Gazi Zibari, John C McDonald Transplant Center, Willis Knighton Medical Center, Shreveport, LA 71103, United States
Wuttiporn Manatsathit, Division of Gastroenterology and Hepatology, University of Nebraska, Omaha, NE 68194, United States
Jonathan Steve Alexander, Department of Molecular and Cellular Physiology, Louisiana State University, School of Medicine, Shreveport, LA 71103, United States
Author contributions: Samant H did literature search and wrote the paper. Manatsathit W, Dies D, Shokouh-Amiri H, Zibari G and Boktor M gave inputs and reviewed it. Alexander JS did critical edit, figures construction and finalize the article.
Conflict-of-interest statement: The authors declare that there is no conflict of interest regarding the publication of this paper.
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/
Corresponding author: Jonathan Steve Alexander, FACG, PhD, Professor, Department of Molecular and Cellular Physiology, Louisiana State University, School of Medicine, 1501 Kings Highway, Shreveport, LA 71103, United States. jalexa@lsuhsc.edu
Telephone: +1-318-6754151 Fax: +1-318-6754156
Received: January 10, 2019 Peer-review started: January 10, 2019 First decision: January 30, 2019 Revised: June 5, 2019 Accepted: June 10, 2019 Article in press: June 10, 2019 Published online: July 6, 2019 Processing time: 177 Days and 15.8 Hours
Abstract
Recently the field of cholestasis has expanded enormously reflecting an improved understanding of the molecular mechanisms underlying bile secretion and its perturbation in chronic cholestatic disease. Novel anti-cholestatic therapeutic options have been developed for patients not favorably responding to ursodeoxycholic acid (UDCA), the current standard treatment for cholestatic liver disease. Important novel treatment targets now also include nuclear receptors involved in bile acid (BA) homoeostasis like farnesoid X receptor and G protein-coupled receptors e.g., the G-protein-coupled BA receptor “transmembrane G coupled receptor 5”. Fibroblast growth factor-19 and enterohepatic BA transporters also deserve attention as additional drug targets as does the potential treatment agent norUDCA. In this review, we discuss recent and future promising therapeutic agents and their potential molecular mechanisms in cholestatic liver disorders.
Core tip: Anti-cholestatic therapeutic options now go beyond ursodeoxycholic acid (UDCA) and target nuclear receptors regulating bile acid (farnesoid X receptor) and G protein-coupled receptor and fibroblast growth factor-19. Additionally, enterohepatic bile acid transporters and norUDCA represent potential targets in cholestatic disease.
