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HPB Surgery
Volume 2012, Article ID 176723, 8 pages
Review Article

Ischemia/Reperfusion Injury in Liver Surgery and Transplantation: Pathophysiology

1Department of Gastroenterology, Endocrinology, Rheumatology and Infectious Diseases, University Hospital Regensburg, D-93053 Regensburg, Germany
2Department of Gastroenterology, University Hospital Heidelberg, D-69120 Heidelberg, Germany
3Department of General and Transplant Surgery, University Hospital Heidelberg, D-69120 Heidelberg, Germany

Received 18 February 2012; Accepted 5 April 2012

Academic Editor: John J. Lemasters

Copyright © 2012 Kilian Weigand et al. 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.


Liver ischemia/reperfusion (IR) injury is caused by a heavily toothed network of interactions of cells of the immune system, cytokine production, and reduced microcirculatory blood flow in the liver. These complex networks are further elaborated by multiple intracellular pathways activated by cytokines, chemokines, and danger-associated molecular patterns. Furthermore, intracellular ionic disturbances and especially mitochondrial disorders play an important role leading to apoptosis and necrosis of hepatocytes in IR injury. Overall, enhanced production of reactive oxygen species, found very early in IR injury, plays an important role in liver tissue damage at several points within these complex networks. Many contributors to IR injury are only incompletely understood so far. This paper tempts to give an overview of the different mechanisms involved in the formation of IR injury. Only by further elucidation of these complex mechanisms IR injury can be understood and possible therapeutic strategies can be improved or be developed.