ArticleToxicology letters2010
The role of damage associated molecular pattern molecules in acetaminophen-induced liver injury in mice.
Article in Toxicology letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
105 citing papers in PubMed, 222 citations in OpenAlex.
- Role of Toll-like receptor 2 and 4 signaling pathways on the inflammatory response to resistance training in elderly subjects.Age (Dordrecht, Netherlands) · 2014Trial
- HBV/HCV coinfection and anti-tuberculosis drug-induced liver injury: from risk assessment and exploration of mechanisms to preventive considerations.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026Review
- Mesenchymal Stromal Cell-Based Cell-Drug Conjugates for the Treatment of Acute Liver Failure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Platelets mediate neutrophil infiltration and exacerbate liver injury and sinusoidal endothelial cell damage after a severe acetaminophen overdose in mice.Archives of toxicology · 2025Article
- Kupffer Cells Regulate iNKT Cells Through Il-12 to Mitigate the Extent of APAP-Induced Damage in the Liver.Journal of cellular and molecular medicine · 2025Article
- Chitinase 3-like protein 1 deficiency ameliorates drug-induced acute liver injury by inhibition of neutrophil recruitment through lipocalin-2.Frontiers in pharmacology · 2025Article
- HMGB1 as an extracellular pro-inflammatory cytokine: Implications for drug-induced organic damage.Cell biology and toxicology · 2024Review
- A liver digital twin for in silico testing of cellular and inter-cellular mechanisms in regeneration after drug-induced damage.iScience · 2024Article
- The Modulation of Phospho-Extracellular Signal-Regulated Kinase and Phospho-Protein Kinase B Signaling Pathways plus Activity of Macrophage-Stimulating Protein Contribute to the Protective Effect of Stachydrine on Acetaminophen-Induced Liver Injury.International journal of molecular sciences · 2024Article
- Acetaminophen Hepatotoxicity: Paradigm for Understanding Mechanisms of Drug-Induced Liver Injury.Annual review of pathology · 2024Review
- The molecular mechanisms of acetaminophen-induced hepatotoxicity and its potential therapeutic targets.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Molecular mechanisms of autophagy and implications in liver diseases.Liver research (Beijing, China) · 2023Review
- Reappraisal of oxidized HMGB1 as a mediator and biomarker.Future science OA · 2022Review
- The immunological mechanisms and therapeutic potential in drug-induced liver injury: lessons learned from acetaminophen hepatotoxicity.Cell & bioscience · 2022Review
- Generation of pro-and anti-inflammatory mediators after acetaminophen overdose in surviving and non-surviving patients.Toxicology letters · 2022Article
- Sapidolide A alleviates acetaminophen-induced acute liver injury by inhibiting NLRP3 inflammasome activation in macrophages.Acta pharmacologica Sinica · 2022Article
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- Hepatoprotective Effect ofFrontiers in pharmacology · 2022Article
- The Timing and Effects of Low-Dose Ethanol Treatment on Acetaminophen-Induced Liver Injury.Life (Basel, Switzerland) · 2021Article
- The COVIDome Explorer researcher portal.Cell reports · 2021Article
45 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The idiosyncratic nature, severity and poor diagnosis of drug-induced liver injury (DILI) make these reactions a major safety issue during drug development, as well as the most common cause for the withdrawal of drugs from the pharmaceutical market. Elucidation of the underlying mechanism(s) is necessary for identifying predisposing factors and developing strategies in the treatment and prevention of DILI. Acetaminophen (APAP) is a widely used over the counter therapeutic that is known to be effective and safe at therapeutic doses. However, in overdose situations fatal and non-fatal hepatic necrosis can result. Evidence suggests that the chemically reactive metabolite of the drug initiates hepatocyte damage and that inflammatory innate immune responses also occur within the liver, leading to the exacerbation and progression of tissue injury. Here we investigate whether following APAP-induced liver injury (AILI) damaged hepatocytes release "danger" signals or damage associated molecular pattern (DAMP) molecules, which induce pro-inflammatory activation of hepatic macrophages, further contributing to the progression of liver injury. Our study demonstrated a clear activation of Kupffer cells following early exposure to APAP (1h). Activation of a murine macrophage cell line, RAW cells, was also observed following treatment with liver perfusate from APAP-treated mice, or with culture supernatant of APAP-challenged hepatocytes. Moreover, in these media, the DAMP molecules, heat-shock protein-70 (HSP-70) and high mobility group box-1 (HMGB1) were detected. Overall, these findings reveal that DAMP molecules released from damaged and necrotic hepatocytes may serve as a crucial link between the initial hepatocyte damage and the activation of innate immune cells following APAP-exposure, and that DAMPs may represent a potential therapeutic target for AILI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.