Molecular biology of liver ischemia/reperfusion injury: established mechanisms and recent advancements.
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.
Klune
John R
JR
Department of Surgery, F675 UPMC Presbyterian Hospital, University of Pittsburgh Medical Center, 200 Lothrop Street, Pittsburgh, PA 15213, USA.
Tsung
Allan
A
D000818:Animals; D017209:Apoptosis; D015415:Biomarkers / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D024243:HMGB1 Protein / Q000378:metabolism*; D022781:Hepatocytes / Q000378:metabolism; D006801:Humans; D008099:Liver / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology; D051197:Toll-Like Receptor 4 / Q000378:metabolism*
D015415:Biomarkers; D016207:Cytokines; D024243:HMGB1 Protein; D017382:Reactive Oxygen Species; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4; D009569:Nitric Oxide