Molecular mechanisms of hepatic ischemia-reperfusion injury and preconditioning.

By H. Jaeschke. American Journal of Physiology - Gastrointestinal and Liver Physiology, 2003

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Role of Kupffer cells in host defense and liver disease (2006, background): “Moreover, the production of a vascular oxidant stress by the NADPH oxidase of KC, has been identified as central pathomechanism of hepatic reperfusion injury which enhances NFkB and activator protein-1 (AP-1)-mediated expression of genes, such as TNF-a, chemokines and adhesion molecules (97).”
OXIDANT STRESS, MITOCHONDRIA AND CELL DEATH MECHANISMS IN DRUG-INDUCED LIVER INJURY: LESSONS LEARNED FROM ACETAMINOPHEN HEPATOTOXICITY (2012, background): “…and recruited neutrophils can be activated and produce ROS and directly, through ROS-mediated mechanisms, can cause liver injury in hepatic ischemia-reperfusion injury, obstructive cholestasis, and various models of endotoxemia (Jaeschke, 2003, 2011; Jaeschke and Hasegawa, 2006) (Figure 3).”
Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME (2013, neutral): “This may have important consequences in terms of tissue damage, since engagement of ICAM-1 by its receptor Mac-1 in neutrophils causes their degranulation and extensive oxidative stress (Jaeschke 2003; Shappell et al. 1990).”