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Ischemia/Reperfusion Injury in Liver Surgery and Transplantation: Pathophysiology
Author(s) -
Kilian Weigand,
S Brost,
Niels Steinebrunner,
Markus W. Büchler,
Peter Schemmer,
Martina Müller
Publication year - 2012
Publication title -
hpb surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.561
H-Index - 26
eISSN - 1607-8462
pISSN - 0894-8569
DOI - 10.1155/2012/176723
Subject(s) - reperfusion injury , medicine , chemokine , liver injury , ischemia , intracellular , liver transplantation , pathophysiology , cytokine , immune system , reactive oxygen species , transplantation , apoptosis , bioinformatics , microbiology and biotechnology , immunology , pharmacology , pathology , biology , biochemistry , surgery
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.

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