ArticleComputational toxicology (Amsterdam, Netherlands)2019
Frequent Modulation of the Sterol Regulatory Element Binding Protein (SREBP) by Chemical Exposure in the Livers of Rats.
Article in Computational toxicology (Amsterdam, Netherlands), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 14 citations in OpenAlex.
- Mechanism-based new approach methodologies for in vitro detection of chemical-induced liver steatosis.Archives of toxicology · 2026Review
- Dose-response modeling of effects in mice after exposure to a polyfluoroalkyl substance (Nafion byproduct 2).Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Article
- Sulforaphane ameliorates bisphenol A-induced hepatic lipid accumulation by inhibiting endoplasmic reticulum stress.Scientific reports · 2023Article
- Exposure to low-dose perfluorooctanoic acid promotes hepatic steatosis and disrupts the hepatic transcriptome in mice.Molecular metabolism · 2022Article
- A Collaborative Initiative to Establish Genomic Biomarkers for Assessing Tumorigenic Potential to Reduce Reliance on Conventional Rodent Carcinogenicity Studies.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Drug-induced hepatic steatosis in absence of severe mitochondrial dysfunction in HepaRG cells: proof of multiple mechanism-based toxicity.Cell biology and toxicology · 2021Article
- Assessment of the Mode of Action Underlying the Effects of GenX in Mouse Liver and Implications for Assessing Human Health Risks.Toxicologic pathology · 2020Article
- Article
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Authors and funding
1 author at 1 institution in 1 country.
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Abstract
Inappropriate activation of sterol regulatory element-binding proteins (SREBPs) can lead to non-alcoholic fatty liver disease (NAFLD). To link chemical exposure to SREBP activity, a previously characterized gene expression biomarker (Rooney et al., 2019) was used to identify microarray comparisons from rat liver that exhibited significant positive or negative correlation to the biomarker. The effects of 620 chemicals on SREBP activity were examined across 9305 chemical-dose-time microarray comparisons. SREBP was found to be frequently modulated by chemical exposure with 54% of the chemicals affecting SREBP activity. Activators included inhibitors of cholesterogenesis that act to inhibit HMG-CoA reductase (statins) or inhibit Cyp51 (conazoles). Most chemical effects were transient, lasting usually no more than 2-4 days. Modulation of SREBP in most cases led to coordinated increases or decreases in lipogenic and cholesterogenic genes. However, 570 chemical exposure conditions were identified in which regulation was uncoupled. Most of these conditions affected cholesterogenic genes in the absence of parallel effects on lipogenic genes. Together, these findings show that SREBP is a frequent target of chemical exposure and expression of lipogenic and cholesterogenic genes can be uncoupled.
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