Abstract
The availability of suitable animal models reproducing at least some of the typical clinical features of acute and chronic liver disease in humans would facilitate studies of liver pathophysiology and the design and evaluation of new treatments. Unfortunately, with the exception of hereditary enzyme deficiencies and acetaminophen poisoning, only a few animal models of liver failure appear to meet this requirement. Additionally, in fulminant hepatic failure (FHF) models, the hepatic injury should be potentially reversible and death should occur within a well-defined interval as the direct consequence of FHF and its complications, including coma and brain swelling. Animal models of hereditary defects of liver metabolism have provided a wealth of information on physiologic, biochemical, and molecular mechanisms of several enzymatic defects. Experiments in defective animals have also contributed to the development of specific therapies (dietary, pharmacologic, gene therapy, replacement by organ and hepatocyte transplantation).
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