Hepatic ischemia reperfusion injury: Contemporary perspectives on pathogenic mechanisms and basis for hepatoprotection-the good, bad and deadly
Date
2011
Authors
Teoh, Narcissus
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Blackwell Publishing Ltd
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.
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Keywords
Keywords: chemokine receptor CXCR4; CXCL1 chemokine; CXCL2 chemokine; CXCL3 chemokine; ferritin; heme oxygenase; interleukin 12; reactive oxygen metabolite; toll like receptor; toll like receptor 1; toll like receptor 10; toll like receptor 2; toll like receptor 3; Chemokines; Heme oxygenase; Hepatocyte cell death; Inflammation; Kupffer cells; Liver ischemia reperfusion injury; Neutrophils; Receptor for Advanced Glycation End Products (RAGE); Toll-Like Receptor (TLR); Tumor necrosis factor-a
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Source
Journal of Gastroenterology and Hepatology
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Journal article
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Restricted until
2037-12-31
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