Hepatic ischemia reperfusion injury: Contemporary perspectives on pathogenic mechanisms and basis for hepatoprotection-the good, bad and deadly

J Gastroenterol Hepatol. 2011 Jan;26 Suppl 1:180-7. doi: 10.1111/j.1440-1746.2010.06584.x.

Abstract

Hepatic ischemia reperfusion (IR) injury is an important clinical problem complicating liver surgery and transplantation. The pathogenesis underlying reperfusion injury after warm ischemia is complex, encompassing a multitude of different cell types and signalling mechanisms innate and/or mobilized to the liver. Since the author's 2003 review in the Journal, considerable progress has been achieved in enhancing our understanding of some of the pathogenic pathways and crucial mediators of hepatic inflammation such as the heme oxygenase system, CXC chemokines, Toll-like receptors as well as the mode of parenchymal cell death in IR injury. A better appreciation of these mechanisms will accelerate efforts in designing optimal interventions to prevent hepatic IR injury and improve outcomes after liver transplantation.

MeSH terms

  • Animals
  • Apoptosis
  • Chemokines, CXC / metabolism
  • Disease Models, Animal
  • Heme Oxygenase (Decyclizing) / metabolism
  • Humans
  • Inflammation Mediators / metabolism
  • Liver / blood supply*
  • Liver / immunology
  • Liver / metabolism
  • Liver Transplantation / adverse effects*
  • Necrosis
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic / metabolism
  • Reperfusion Injury / etiology
  • Reperfusion Injury / immunology
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / prevention & control*
  • Signal Transduction
  • Toll-Like Receptors / metabolism
  • Warm Ischemia / adverse effects*

Substances

  • Chemokines, CXC
  • Inflammation Mediators
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic
  • Toll-Like Receptors
  • Heme Oxygenase (Decyclizing)