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Author Maes, Michaël ♦ Vinken, Mathieu ♦ Jaeschke, Hartmut
Source United States Department of Energy Office of Scientific and Technical Information
Content type Text
Language English
Subject Keyword APPLIED LIFE SCIENCES ♦ ALANINES ♦ AMINOTRANSFERASES ♦ BENZOQUINONES ♦ CONCANAVALIN A ♦ ENDOTOXINS ♦ FAILURES ♦ GLUTATHIONE ♦ HEPATITIS ♦ IMINES ♦ INJURIES ♦ INTERFERON ♦ LIGANDS ♦ LIVER ♦ NECROSIS ♦ NEOPLASMS ♦ PHOSPHOTRANSFERASES ♦ RECEPTORS ♦ SURGERY
Abstract Acute liver failure can be the consequence of various etiologies, with most cases arising from drug-induced hepatotoxicity in Western countries. Despite advances in this field, the management of acute liver failure continues to be one of the most challenging problems in clinical medicine. The availability of adequate experimental models is of crucial importance to provide a better understanding of this condition and to allow identification of novel drug targets, testing the efficacy of new therapeutic interventions and acting as models for assessing mechanisms of toxicity. Experimental models of hepatotoxicity related to acute liver failure rely on surgical procedures, chemical exposure or viral infection. Each of these models has a number of strengths and weaknesses. This paper specifically reviews commonly used chemical in vivo and in vitro models of hepatotoxicity associated with acute liver failure. - Highlights: • The murine APAP model is very close to what is observed in patients. • The Gal/ET model is useful to study TNFα-mediated apoptotic signaling mechanisms. • Fas receptor activation is an effective model of apoptosis and secondary necrosis. • The ConA model is a relevant model of auto-immune hepatitis and viral hepatitis. • Multiple time point evaluation needed in experimental models of acute liver injury.
ISSN 0041008X
Educational Use Research
Learning Resource Type Article
Publisher Date 2016-01-01
Publisher Place United States
Journal Toxicology and Applied Pharmacology
Volume Number 290


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