ArticleThe Journal of pharmacology and experimental therapeutics2011
The role of hypoxia-inducible factor-1α in acetaminophen hepatotoxicity.
Article in The Journal of pharmacology and experimental therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 44 citations in OpenAlex.
- Edible Fungus Compound Cordycepin Protects Against Acetaminophen-Induced Liver Injury.Journal of clinical laboratory analysis · 2026Article
- Exosome-niosome hybrid oxygen carrier for protection against acetaminophen-induced acute liver injury.Biomaterials science · 2026Article
- Hepatic Hypoxia-Inducible Factor 1α Mediates Ferroptosis via Transferrin Receptor 1 in Acute Liver Injury.Antioxidants (Basel, Switzerland) · 2026Article
- [Progress in clinical research on potential therapeutic drugs for acute-on-chronic liver failure].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023Article
- CB2R agonist GW405833 alleviates acute liver failure in mice via inhibiting HIF-1α-mediated reprogramming of glycometabolism and macrophage proliferation.Acta pharmacologica Sinica · 2023Article
- Regulatory mechanism of HIF-1α and its role in liver diseases: a narrative review.Annals of translational medicine · 2022Review
- Review
- BRG1 Links TLR4 Trans-Activation to LPS-Induced SREBP1a Expression and Liver Injury.Frontiers in cell and developmental biology · 2021Article
- Article
- Hepatic dysfunction and thrombocytopenia induced by excess sFlt1 in mice lacking endothelial nitric oxide synthase.Scientific reports · 2018Article
- Liquid chromatography mass spectrometry-based profiling of phosphatidylcholine and phosphatidylethanolamine in the plasma and liver of acetaminophen-induced liver injured mice.Lipids in health and disease · 2017Article
- Role of Hypoxia-Inducible Factors in the Development of Liver Fibrosis.Cellular and molecular gastroenterology and hepatology · 2015Review
- Serotonin deficiency exacerbates acetaminophen-induced liver toxicity in mice.Scientific reports · 2015Article
- Article
- Hepatic stellate cells orchestrate clearance of necrotic cells in a hypoxia-inducible factor-1α-dependent manner by modulating macrophage phenotype in mice.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Article
- Age-related decrease in cerebrovascular-derived neuroprotective proteins: effect of acetaminophen.Microvascular research · 2012Article
- Effect of trifluoperazine on toxicity, HIF-1α induction and hepatocyte regeneration in acetaminophen toxicity in mice.Toxicology and applied pharmacology · 2012Article
- YC-1 exerts inhibitory effects on MDA-MB-468 breast cancer cells by targeting EGFR in vitro and in vivo under normoxic condition.Chinese journal of cancer · 2012Article
- Hypoxia and hypoxia inducible factors: diverse roles in liver diseases.Hepatology (Baltimore, Md.) · 2012Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Hypoxia-inducible factor-1α (HIF-1α) is a critical transcription factor that controls oxygen homeostasis in response to hypoxia, inflammation, and oxidative stress. HIF has been implicated in the pathogenesis of liver injury in which these events play a role, including acetaminophen (APAP) overdose, which is the leading cause of acute liver failure in the United States. APAP overdose has been reported to activate HIF-1α in mouse livers and isolated hepatocytes downstream of oxidative stress. HIF-1α signaling controls many factors that contribute to APAP hepatotoxicity, including mitochondrial cell death, inflammation, and hemostasis. Therefore, we tested the hypothesis that HIF-1α contributes to APAP hepatotoxicity. Conditional HIF-1α deletion was generated in mice using an inducible Cre-lox system. Control (HIF-1α-sufficient) mice developed severe liver injury 6 and 24 h after APAP overdose (400 mg/kg). HIF-1α-deficient mice were protected from APAP hepatotoxicity at 6 h, but developed severe liver injury by 24 h, suggesting that HIF-1α is involved in the early stage of APAP toxicity. In further studies, HIF-1α-deficient mice had attenuated thrombin generation and reduced plasminogen activator inhibitor-1 production compared with control mice, indicating that HIF-1α signaling contributes to hemostasis in APAP hepatotoxicity. Finally, HIF-1α-deficient animals had decreased hepatic neutrophil accumulation and plasma concentrations of interleukin-6, keratinocyte chemoattractant, and regulated upon activation normal T cell expressed and secreted compared with control mice, suggesting an altered inflammatory response. HIF-1α contributes to hemostasis, sterile inflammation, and early hepatocellular necrosis during the pathogenesis of APAP toxicity.
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