Molecular biology of liver ischemia/reperfusion injury: established mechanisms and recent advancements

Surg Clin North Am. 2010 Aug;90(4):665-77. doi: 10.1016/j.suc.2010.04.003.


Hepatic ischemia/reperfusion (I/R) injury occurs in a variety of clinical contexts, including transplantation, liver resection surgery, trauma, and hypovolemic shock. The mechanism of organ damage after I/R has been studied extensively and consists of complex interactions of multiple inflammatory pathways. The major contributors to I/R injury include production of reactive oxygen species, release of proinflammatory cytokines and chemokines, and activation of immune cells to promote inflammation and tissue damage. Recent research has focused on the mechanisms by which these immune responses are initially activated through signaling molecules and their cellular receptors. Thorough understanding of the pathophysiology of liver I/R may yield novel therapeutic strategies to reduce I/R injury and lead to improved clinical outcomes.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis
  • Biomarkers / metabolism
  • Cytokines / metabolism
  • HMGB1 Protein / metabolism*
  • Hepatocytes / metabolism
  • Humans
  • Liver / blood supply*
  • Liver / metabolism
  • Liver / pathology
  • Nitric Oxide / metabolism
  • Oxidative Stress / physiology*
  • Reactive Oxygen Species / metabolism*
  • Reperfusion Injury / metabolism*
  • Reperfusion Injury / pathology
  • Toll-Like Receptor 4 / metabolism*


  • Biomarkers
  • Cytokines
  • HMGB1 Protein
  • Reactive Oxygen Species
  • TLR4 protein, human
  • Toll-Like Receptor 4
  • Nitric Oxide