ArticleCommunications biology2024
Downregulation of HNF4A enables transcriptomic reprogramming during the hepatic acute-phase response.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Tumor-derived Parathyroid Hormone-Related Protein Is Associated with Suppression of Cytochrome P450 Expression: Evidence From Multimodal Transcriptomics.ACS pharmacology & translational science · 2026Article
- An explainable machine learning method for identifying key atherogenic lipid biomarkers in abdominal obesity among the Southern Chinese population.Lipids in health and disease · 2026Article
- HepG2 cells stimulated by THP-1-conditioned medium: a potential in vitro model of systemic inflammation-induced hepatic alterations.Molecular biology reports · 2026Article
- Review
- SAMHD1 depletion restricts SARS-CoV-2 infection by suppressing HNF1-dependent ACE2 expression in lung epithelial cells.PLoS pathogens · 2026Article
- Circulating Liver-Enriched miR-122 in COVID-19 Patients: A Longitudinal Real-Life Study.International journal of molecular sciences · 2026Article
- Diurnal Regulation and Gene-Specific Vulnerability of Oxidative Alcohol-Metabolizing Enzymes to Circadian Disruption.International journal of molecular sciences · 2026Article
- Transcriptomic Profile of Directed Differentiation of iPSCs into Hepatocyte-like Cells.International journal of molecular sciences · 2026Article
- Review
- The Wnt/β-catenin-P2-HNF4α feedback loop facilitates colorectal tumorigenesis and malignancy.Journal of translational medicine · 2025Article
- SAMHD1 promotes SARS-CoV-2 infection by enhancing HNF1-dependent ACE2 expression in lung epithelial cells.bioRxiv : the preprint server for biology · 2025Article
- Article
- Hepatocyte nuclear factor 4-Alpha: a key regulator in liver carcinogenesis.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Loss of SVIP Results in Metabolic Reprograming and Increased Retention of Very-Low-Density Lipoproteins in Hepatocytes.International journal of molecular sciences · 2025Article
- Characterization of non-coding variants associated with transcription-factor binding through ATAC-seq-defined footprint QTLs in liver.American journal of human genetics · 2025Article
- Downregulation of the NF-κB protein p65 is a shared phenotype among most anti-aging interventions.GeroScience · 2025Article
- Hepatocyte Nuclear Factor 4 Alpha: A Key Regulator of Liver Disease Pathology and Haemostatic Disorders.Liver international : official journal of the International Association for the Study of the Liver · 2025Review
- HNF4A mitigates sepsis-associated lung injury by upregulating NCOR2/GR/STAB1 axis and promoting macrophage polarization towards M2 phenotype.Cell death & disease · 2025Article
- TLR4 modulates simvastatin's impact on HDL cholesterol and glycemic control.Frontiers in pharmacology · 2025Article
- Combined Analysis of Transcriptome and Mendelian Randomization RevealsJournal of inflammation research · 2025Article
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8 authors.
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Abstract
The hepatic acute-phase response is characterized by a massive upregulation of serum proteins, such as haptoglobin and serum amyloid A, at the expense of liver homeostatic functions. Although the transcription factor hepatocyte nuclear factor 4 alpha (HNF4A) has a well-established role in safeguarding liver function and its cistrome spans around 50% of liver-specific genes, its role in the acute-phase response has received little attention so far. We demonstrate that HNF4A binds to and represses acute-phase genes under basal conditions. The reprogramming of hepatic transcription during inflammation necessitates loss of HNF4A function to allow expression of acute-phase genes while liver homeostatic genes are repressed. In a pre-clinical liver organoid model overexpression of HNF4A maintained liver functionality in spite of inflammation-induced cell damage. Conversely, HNF4A overexpression potently impaired the acute-phase response by retaining chromatin at regulatory regions of acute-phase genes inaccessible to transcription. Taken together, our data extend the understanding of dual HNF4A action as transcriptional activator and repressor, establishing HNF4A as gatekeeper for the hepatic acute-phase response.
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