ArticleMolecular and cellular biology2012
The hypoxia-inducible factor-C/EBPα axis controls ethanol-mediated hepcidin repression.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- High‑altitude polycythemia: Unveiling the molecular landscape beyond erythropoietin (Review).International journal of molecular medicine · 2026Review
- Hepatic Hamp restoration contributes to nicotinamide mononucleotide (NMN)-alleviated hepatic steatosis in chronic alcohol-fed mice.Communications biology · 2026Article
- Impaired iron balance and erythrocytosis: a complex relationship.Blood cancer journal · 2026Review
- TFR2 p.A75V mutation aggravates liver iron overload in alcoholic liver disease via ERK pathway.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Excessive intake of fructose and alcohol aggravates high-fat diet-induced steatohepatitis and changes hepatic iron homeostasis.Histochemistry and cell biology · 2025Article
- Fetal Alcohol Spectrum Disorder and Iron Homeostasis.Nutrients · 2022Review
- Novel Insights into Alcoholic Liver Disease: Iron Overload, Iron Sensing and Hemolysis.Journal of translational internal medicine · 2022Article
- Crosstalk between Oxidative Stress and Inflammatory Liver Injury in the Pathogenesis of Alcoholic Liver Disease.International journal of molecular sciences · 2022Review
- SMAD family member 3 (SMAD3) and SMAD4 repress HIF2α-dependent iron-regulatory genes.The Journal of biological chemistry · 2019Article
- Role of HIF-1α in Alcohol-Mediated Multiple Organ Dysfunction.Biomolecules · 2018Review
- Hypoxia enhances HRedox biology · 2018Article
- Maternal iron nutriture as a critical modulator of fetal alcohol spectrum disorder risk in alcohol-exposed pregnancies.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2018Review
- Activation of intestinal hypoxia-inducible factor 2α during obesity contributes to hepatic steatosis.Nature medicine · 2017Article
- Review
- Pattern analysis uncovers a chronic ethanol-induced disruption of the switch-like dynamics of C/EBP-β and C/EBP-α genome-wide binding during liver regeneration.Physiological genomics · 2017Article
- Hepcidin inhibits Smad3 phosphorylation in hepatic stellate cells by impeding ferroportin-mediated regulation of Akt.Nature communications · 2016Article
- HIF2α Is an Essential Molecular Brake for Postprandial Hepatic Glucagon Response Independent of Insulin Signaling.Cell metabolism · 2016Article
- Mechanisms of divalent metal toxicity in affective disorders.Toxicology · 2016Review
- New advances in molecular mechanisms and emerging therapeutic targets in alcoholic liver diseases.World journal of gastroenterology · 2014Review
- Loss of von Hippel-Lindau protein (VHL) increases systemic cholesterol levels through targeting hypoxia-inducible factor 2α and regulation of bile acid homeostasis.Molecular and cellular biology · 2014Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Hepcidin is a liver-derived peptide hormone and the master regulator of systemic iron homeostasis. Decreased hepcidin expression is a common feature in alcoholic liver disease (ALD) and in mouse models of ethanol loading. Dysregulation of hepcidin signaling in ALD leads to liver iron deposition, which is a major contributing factor to liver injury. The mechanism by which hepcidin is regulated following ethanol treatment is unclear. An increase in liver hypoxia was observed in an acute ethanol-induced liver injury model. The hypoxic response is controlled by a family of hypoxia-inducible transcription factors (HIFs), which are composed of an oxygen-regulated alpha subunit (HIFα) and a constitutively present beta subunit, aryl hydrocarbon receptor nuclear translocator (HIFβ/Arnt). Disruption of liver HIF function reversed the repression of hepcidin following ethanol loading. Mouse models of liver HIF overexpression demonstrated that both HIF-1α and HIF-2α contribute to hepcidin repression in vivo. Ethanol treatment led to a decrease in CCAAT-enhancer-binding protein alpha (C/EBPα) protein expression in a HIF-dependent manner. Importantly, adenoviral rescue of C/EBPα in vivo ablated the hepcidin repression in response to ethanol treatment or HIF overexpression. These data provide novel insight into the regulation of hepcidin by hypoxia and indicate that targeting HIFs in the liver could be therapeutic in ALD.
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