ArticleScientific reports2017
Role of HDAC9-FoxO1 Axis in the Transcriptional Program Associated with Hepatic Gluconeogenesis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Integrated Multi-Omics Analysis and Experimental Validation Identify Acetylation-Related Genes as Potential Regulators in Osteoarthritis.Biomedicines · 2026Article
- Hepatic Glucocorticoid Receptor Action and Glucose Homeostasis.Endocrine reviews · 2026Review
- The multifactorial role of HDAC9 at the maternal-fetal interface in the pathogenesis of preeclampsia.Clinical science (London, England : 1979) · 2025Review
- FOXO1 phosphorylation as a context-dependent molecular switch in cancer: from mechanisms to precision therapy.World journal of surgical oncology · 2025Review
- Effect of HDAC9-induced deacetylation of glycolysis-related GAPDH lysine 219 on rotavirus replication in rotavirus-infected Caco-2 cells.Virus genes · 2024Article
- Identification of HDAC9 and ARRDC4 as potential biomarkers and targets for treatment of type 2 diabetes.Scientific reports · 2024Article
- HDAC9 as a Privileged Target: Reviewing its Role in Different Diseases and Structure-activity Relationships (SARs) of its Inhibitors.Mini reviews in medicinal chemistry · 2024Review
- Molecular mechanism and therapeutic potential of HDAC9 in intervertebral disc degeneration.Cellular & molecular biology letters · 2023Article
- Metabolic Reprogramming of HCC: A New Microenvironment for Immune Responses.International journal of molecular sciences · 2023Review
- The Effects of Viruses on Insulin Sensitivity and Blood-Brain Barrier Function.International journal of molecular sciences · 2023Review
- Stroke by inducing HDAC9-dependent deacetylation of HIF-1 and Sp1, promotes TfR1 transcription and GPX4 reduction, thus determining ferroptotic neuronal death.International journal of biological sciences · 2023Article
- Histone deacetylase (HDAC) 9: versatile biological functions and emerging roles in human cancer.Cellular oncology (Dordrecht, Netherlands) · 2021Review
- Review
- Quis Custodiet Ipsos Custodes (Who Controls the Controllers)? Two Decades of Studies on HDAC9.Life (Basel, Switzerland) · 2021Review
- Metabolic alterations and vulnerabilities in hepatocellular carcinoma.Gastroenterology report · 2021Review
- Forkhead Box Protein O1: Functional Diversity and Post-Translational Modification, a New Therapeutic Target?Drug design, development and therapy · 2021Review
- What turns CREB on? And off? And why does it matter?Cellular and molecular life sciences : CMLS · 2020Review
- Histone Deacetylase 9: Its Role in the Pathogenesis of Diabetes and Other Chronic Diseases.Diabetes & metabolism journal · 2020Review
- Histone Deacetylases in Kidney Physiology and Acute Kidney Injury.Seminars in nephrology · 2020Review
- Understanding Failure and Improving Treatment Using HDAC Inhibitors for Prostate Cancer.Biomedicines · 2020Review
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylase 9 (HDAC9) regulates hepatic gluconeogenesis by deacetylating Forkhead box O 1 (FoxO1). HDAC9 upregulation is involved in hepatitis C virus (HCV)-associated exaggerated gluconeogenesis. Herein, we found in addition to FoxO1, HDAC9 also regulates other gluconeogenic transcription factors, including peroxisomeproliferator-activated receptor-γ coactivator-1α (PGC-1α), cyclic AMP-responsive element-binding protein (CREB), and glucocorticoid receptor (GR). Unlike FoxO1, which is regulated by post-translational modification responses to HDAC9, HDAC9 regulates PGC-1α, CREB and GR by altering gene expression. Similar to PGC-1α, CREB and GR were found to be novel regulatory targets of FoxO1 by examination of the FoxO1 binding site in their promoter. PGC-1α, CREB and GR were upregulated in response to HDAC9 via FoxO1 deacetylation. These findings indicate that HDAC9-FoxO1 signalling contributes to gluconeogenesis by modulating the expression of gluconeogenic transcription factors. In particular, metabolic profiling demonstrated a clear shift towards gluconeogenesis metabolism, and HDAC9-FoxO1 signalling can be strongly induced to upregulate gluconeogenic transcription factors following HCV infection. The positive correlation between HDAC9 and gluconeogenic transcription factor expression levels in the livers of both HCV-infected patients and normal individuals further emphasizes the clinical relevance of these results. Thus, HDAC9-FoxO1 signalling axis is involved in regulating gluconeogenic transcription factors, gluconeogenesis, and HCV-induced type 2 diabetes.
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