Figure 1.

Molecular pathophysiology of liver I/R and the sterile immune response. Hepatocytes unable to cope with extensive ROS production undergo necrotic cell death and release DAMPs. These DAMPs activate Kupffer cells, leading to production of ROS, chemokines and cytokines that recruit additional leukocytes directly or via activated sinusoidal endothelial cells. The chemoattracted leukocytes (mainly monocytes and neutrophils) amplify ROS production, thereby inducing parenchymal necrosis and additional DAMP release. The shown processes should be interpreted in a cyclical manner and are reviewed in detail elsewhere (8,9).