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Journal of Transplantation
Volume 2012, Article ID 164329, 17 pages
http://dx.doi.org/10.1155/2012/164329
Review Article

Ischemia-Reperfusion Injury and Ischemic-Type Biliary Lesions following Liver Transplantation

1Service de Chirurgie et Transplantation Hépatique, Hôpital l'Archet 2, Centre Hospitalier Universitaire de Nice, Université de Nice Sophia-Antipolis, 151 Route Saint Antoine de Ginestière, B.P. 3079, 06202 Nice Cedex 2, France
2INSERM U526, Equipe 2: Cell Death, Differentiation and Cancer, Centre Méditerranéen de Médecine Moléculaire, Bâtiment Universitaire ARCHIMED, Université de Nice Sophia-Antipolis, 151 Route Saint Antoine de Ginestière, B.P. 2 3194, 06204 Nice Cedex 3, France

Received 14 September 2011; Revised 19 December 2011; Accepted 23 December 2011

Academic Editor: Maciej Kosieradzki

Copyright © 2012 Raffaele Cursio and Jean Gugenheim. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Ischemia-reperfusion (I-R) injury after liver transplantation (LT) induces intra- and/or extrahepatic nonanastomotic ischemic-type biliary lesions (ITBLs). Subsequent bile duct stricture is a significant cause of morbidity and even mortality in patients who underwent LT. Although the pathogenesis of ITBLs is multifactorial, there are three main interconnected mechanisms responsible for their formation: cold and warm I-R injury, injury induced by cytotoxic bile salts, and immunological-mediated injury. Cold and warm ischemic insult can induce direct injury to the cholangiocytes and/or damage to the arterioles of the peribiliary vascular plexus, which in turn leads to apoptosis and necrosis of the cholangiocytes. Liver grafts from suboptimal or extended-criteria donors are more susceptible to cold and warm I-R injury and develop more easily ITBLs than normal livers. This paper, focusing on liver I-R injury, reviews the risk factors and mechanisms leading to ITBLs following LT.