ArticleBiochemical pharmacology2016
Transcription factor binding site enrichment analysis predicts drivers of altered gene expression in nonalcoholic steatohepatitis.
Article in Biochemical pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- ZNF143 inhibits hepatocyte mitophagy and promotes non-alcoholic fatty liver disease by targeting increased lncRNA NEAT1 expression to activate ROCK2 pathway.Epigenetics · 2023Article
- Transcriptional control by HNF-1: Emerging evidence showing its role in lipid metabolism and lipid metabolism disorders.Genes & diseases · 2022Review
- The Chromatin Accessibility Landscape of Nonalcoholic Fatty Liver Disease Progression.Molecules and cells · 2022Article
- Perturbation of Wnt/β-catenin signaling and sexual dimorphism in non-alcoholic fatty liver disease.Hepatology research : the official journal of the Japan Society of Hepatology · 2022Article
- mRNA-miRNA-lncRNA Regulatory Network in Nonalcoholic Fatty Liver Disease.International journal of molecular sciences · 2021Article
- The Gene Signature Associated with Hepatocellular Carcinoma in Patients with Nonalcoholic Fatty Liver Disease.Journal of oncology · 2021Article
- Emergent Properties of the HNF4α-PPARγ Network May Drive Consequent Phenotypic Plasticity in NAFLD.Journal of clinical medicine · 2020Article
- rs953413 Regulates Polyunsaturated Fatty Acid Metabolism by Modulating ELOVL2 Expression.iScience · 2020Article
- Molecular and ultrastructure study of endoplasmic reticulum stress in hepatic steatosis: role of hepatocyte nuclear factor 4α and inflammatory mediators.Histochemistry and cell biology · 2020Article
- Proteomic Analysis Reveals Novel Mechanisms by Which Polychlorinated Biphenyls Compromise the Liver Promoting Diet-Induced Steatohepatitis.Journal of proteome research · 2019Article
- Asking the Right Questions With Animal Models: Methionine- and Choline-Deficient Model in Predicting Adverse Drug Reactions in Human NASH.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Article
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
The molecular mechanisms behind the transition from simple steatosis to nonalcoholic steatohepatitis (NASH) in nonalcoholic fatty liver disease (NAFLD) are not clearly understood. This hinders development of effective therapies for treatment and prevention of NASH. In this study expression profiling data from normal, steatosis, and NASH human livers were used to predict transcription factors that are misregulated as mechanistic features of NAFLD progression. Previously-published human NAFLD gene expression profiling data from normal, steatosis, and NASH livers were subjected to transcription factor binding site enrichment analysis. Selected transcription factors that bind enriched transcription factor binding sites were analyzed for changes in expression. Distinct transcription factor binding sites were enriched in genes significantly up- or down-regulated in NASH livers. Those enriched in up-regulated genes were bound by transcription factors such as FOXA, CEBP, and HNF1 family members, while those enriched in down-regulated genes were bound by nuclear receptors involved in xenobiotic sensing and lipid metabolism. Levels of mRNA and protein for selected transcription factors were significantly changed during disease progression. The study indicates that NAFLD progression involves changes in activity or expression of transcription factors that regulate genes involved in hepatic processes known to be altered in NASH. Transcription factors such as PPAR receptors, FoxA family members, and HNF4A might be targeted therapeutically to prevent NAFLD progression.
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