ArticleLiver international : official journal of the International Association for the Study of the Liver2025
Keap1 Deletion Rescues Cell Death Associated With Gpx4 Loss in Hepatocytes During Acute Liver Injury.
Article in Liver international : official journal of the International Association for the Study of the Liver, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Peroxiredoxin II as a metabolic gatekeeper against aflatoxin BMycotoxin research · 2026Article
- Experimental workflows for the accurate identification of mitochondrial redox events.Redox biology · 2026Review
- GATA2 deficiency exacerbates chronic liver injuryWorld journal of stem cells · 2026Article
- Ferroptosis in diabetic retinopathy: from pathogenic mechanisms to translational prospects.Frontiers in endocrinology · 2026Review
- Exploring the inflammatory origins of gouty arthritis: mechanistic studies based on local lesion proteomics and validation.Frontiers in immunology · 2026Article
- Ferroptosis in liver fibrosis and its potential intervention strategy.Cell biology and toxicology · 2025Review
- Keap1 Deletion Rescues Cell Death Associated With Gpx4 Loss in Hepatocytes During Acute Liver Injury.Liver international : official journal of the International Association for the Study of the Liver · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
BACKGROUND &
aimsAcute liver failure (ALF) is a life-threatening condition with limited treatment options beyond liver transplantation in non-acetaminophen cases. The extensive loss of liver function results from severe hepatocyte death, where elevated reactive oxygen species (ROS) play a significant role. Nuclear factor erythroid-2 like 2 (Nrf2) is crucial in ROS defence by regulating genes like glutathione peroxidase 4 (GPX4), which prevents lipid peroxidation (LPO). GPX4 is involved in several regulated cell processes, including apoptosis and ferroptosis.
methodsGPX4 expression was measured in liver samples from healthy, ALF, and acute-on-chronic liver failure (ACLF) patients. To investigate GPX4's role, mice with hepatocyte-specific deletion of Gpx4 (Gpx4
resultsALF patients exhibited reduced GPX4 levels compared to healthy individuals and ACLF patients, consistent with observations in CCl
conclusionOur results demonstrate that Gpx4 plays a critical role in ALF as its absence exacerbates apoptosis. Activating Keap1-dependent pathways targeting antioxidant defence systems and upregulating BCL2 provides substantial protection against ALF in mice lacking Gpx4 in hepatocytes. Our findings suggest that the Keap1-Nrf2 axis is a promising therapeutic target in ALF.
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Registered trials
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