Figure 8. Model of intrahepatic vascular coagulation and epithelial cell apoptosis dynamics in response to FasL.

The early stages of FasL-induced liver injury are manifested by limited hepatocytes apoptosis and intrahepatic vascular coagulation. This is followed at the intermediate stages by a near-concurrent marked increase in liver caspase activation, epithelial apoptosis and intravascular coagulation. The IC is manifested by the formation of FIB-γ dimers and HMW products within the liver, in association with a dramatic shift of FIB-γ from plasma to liver. During the late stages that follow FasL exposure, IC remains relatively unchanged while hepatocytes apoptosis continues. Heparin provides a therapeutic modality that not only limits the extensive of FasL-related liver injury when given as prophylactic but also limits the extent of injury if given at the early stages of injury exposure.