Aller MA, Arias N, Peral I, García-Higarza S, Arias JL, Arias J. Embrionary way to create a fatty liver in portal hypertension. World J Gastrointest Pathophysiol 2017; 8(2): 39-50 [PMID: 28573066 DOI: 10.4291/wjgp.v8.i2.39]
Corresponding Author of This Article
Maria-Angeles Aller, MD, PhD, Department of Surgery, School of Medicine, Complutense University of Madrid, Plaza de Ramón y Cajal s.n., 28040 Madrid, Spain. maaller@med.ucm.es
Research Domain of This Article
Gastroenterology & Hepatology
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/
Maria-Angeles Aller, Isabel Peral, Jaime Arias, Department of Surgery, School of Medicine, Complutense University of Madrid, 28040 Madrid, Spain
Natalia Arias, UCL Division of Medicine, Institute for Liver and Digestive Health, London NW3 2PF, United Kingdom
Sara García-Higarza, Jorge-Luis Arias, Laboratory of Neuroscience, Department of Psychology, University of Oviedo, 33003 Asturias, Spain
Author contributions: Aller MA, Arias N and Arias J wrote the manuscript; Peral I, García-Higarza S and Arias JL contributed to the manuscript by providing intellectual input, and have participated in preparing the manuscript and approved its final version.
Supported by FICYT FC-15-GRUPIN 14-088 and Alfonso Martin Escudero Foundation.
Conflict-of-interest statement: The authors declare that there are any conflict of interest.
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: Maria-Angeles Aller, MD, PhD, Department of Surgery, School of Medicine, Complutense University of Madrid, Plaza de Ramón y Cajal s.n., 28040 Madrid, Spain. maaller@med.ucm.es
Telephone: +34-91-3941388 Fax: +34-91-3947115
Received: December 5, 2016 Peer-review started: December 7, 2016 First decision: January 16, 2017 Revised: February 3, 2017 Accepted: February 28, 2017 Article in press: March 2, 2017 Published online: May 15, 2017 Processing time: 161 Days and 7.7 Hours
Core Tip
Core tip: The current hypothesis proposes that the re-expression of two embryonic systemic functional axes in the rat after partial portal vein ligation produces a non-alcoholic fatty liver disease. These axes, a coelomicamniotic axis and a trophoblastic yolk-sac or vitelline axis, would then integrate in the interstitial liver space of Disse. If so, these recapitulated embryonic functions would produce firstly, the evolution of liver steatosis. In this way, this fat liver could represent a yolk-saclike in portal hypertensive rats. After that, these embryonic functions would induce a gastrulation-like response in which liver fibrosis occcur. For that reason, studying the mechanisms involved in embryonic development could provide key results for a better understanding of the non-alcoholic fatty liver disease pathophysiology.
