This article is part of the supplement: Proceedings of the First International Conference on Toxicogenomics Integrated with Environmental Sciences (TIES-2007)
Systems biology for identifying liver toxicity pathways
1 Cellular and Molecular Biology Lab, Department of Chemical Engineering and Materials Science, Michigan State University, East Lansing, MI 48824, USA
2 Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI 48824, USA
3 Department of Computer Science and Engineering, Michigan State University, East Lansing, MI 48824, USA
4 Biomedical engineering department, Boston University, Boston, MA, 02215, USA
BMC Proceedings 2009, 3(Suppl 2):S2 doi:10.1186/1753-6561-3-S2-S2Published: 10 March 2009
Drug-induced liver toxicity is one of the leading causes of acute liver failure in the United States, exceeding all other causes combined. The objective of this paper is to describe systems biology methods for identifying pathways involved in liver toxicity induced by free fatty acids (FFA) and tumor necrosis factor (TNF)-α in human hepatoblastoma cells (HepG2/C3A). Systems biology approaches were developed to integrate multi-level data, i.e., gene expression, metabolite profile, toxicity measurements and a priori knowledge to identify gene targets for modulating liver toxicity. Targets that modulate liver toxicity, in vitro, were computationally predicted and some targets were experimentally validated.