ReviewLiver international : official journal of the International Association for the Study of the Liver2012
Acetaminophen hepatotoxicity and repair: the role of sterile inflammation and innate immunity.
Review in Liver international : official journal of the International Association for the Study of the Liver, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 208 papers.
What it found
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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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
208 citing papers in PubMed, 465 citations in OpenAlex.
- Blood gene expression profiling of an early acetaminophen response.The pharmacogenomics journal · 2017Trial
- High Doses of N-Acetyl-P-Aminophenol Cause Acute Changes in Electroencephalographic and Electrocardiographic Activities in Wistar Rats.Basic & clinical pharmacology & toxicology · 2026Article
- The Role of Systemic Inflammation in Paracetamol Poisoning-An Experimental Model.International journal of molecular sciences · 2026Article
- TLR9-mediated innate immune signaling contributes to acetaminophen-induced injury in the developing lung.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Pharmacological inhibition of G protein-coupled receptor kinase 2 (GRK2) by paroxetine attenuates acetaminophen-induced hepatotoxicity.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Article
- ATP and Liv-52 Ameliorate Linezolid-Induced Liver Injury via Modulation of NF-κB/NLRP3 Pathways.Biomedicines · 2026Article
- Varied Effects of Carnosine and an Antioxidant-Enriched Carnosine Supplement in Paracetamol-Induced Hepatotoxicity Model in Mice.Current issues in molecular biology · 2026Article
- Syringaresinol alleviates acetaminophen-induced hepatocyte ferroptosis through the Nrf2/HO-1 pathway by targeting Caveolin-1.Chinese medicine · 2026Article
- An ESIPT-AIE nanosensor for ONOOJournal of nanobiotechnology · 2026Article
- Subchronic Alcohol Exposure Exacerbates Acetaminophen-Induced Acute Liver Injury via Macrophage-Mediated Inflammation and Mitochondrial Dysfunction.Mediators of inflammation · 2026Article
- Lipid metabolism orchestrates liver regeneration: an integrated metabolic network.Journal of translational medicine · 2025Review
- Insights into medication-induced liver injury: Understanding and management strategies.Toxicology reports · 2025Review
- Underlying mechanisms and treatment of acetaminophen‑induced liver injury (Review).Molecular medicine reports · 2025Review
- Orientin: a comprehensive review of a promising bioactive flavonoid.Inflammopharmacology · 2025Review
- Engineered mesenchymal stromal cells with bispecific polyvalent peptides suppress excessive neutrophil infiltration and boost therapy.Science advances · 2025Article
- Drug-Induced Liver Injury-Pharmacological Spectrum Among Children.International journal of molecular sciences · 2025Review
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- Molecular mechanisms in liver repair and regeneration: from physiology to therapeutics.Signal transduction and targeted therapy · 2025Review
- D-glucaro-1,4-lactone alleviates acetaminophen-induced hepatotoxicity in mice via modulating gut microbiota and metabolites associated withFrontiers in pharmacology · 2025Article
148 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Acetaminophen (APAP) hepatotoxicity because of overdose is the most frequent cause of acute liver failure in the western world. Metabolic activation of APAP and protein adduct formation, mitochondrial dysfunction, oxidant stress, peroxynitrite formation and nuclear DNA fragmentation are critical intracellular events in hepatocytes. However, the early cell necrosis causes the release of a number of mediators such as high-mobility group box 1 protein, DNA fragments, heat shock proteins (HSPs) and others (collectively named damage-associated molecular patterns), which can be recognized by toll-like receptors on macrophages, and leads to their activation with cytokine and chemokine formation. Although pro-inflammatory mediators recruit inflammatory cells (neutrophils, monocytes) into the liver, neither the infiltrating cells nor the activated resident macrophages cause any direct cytotoxicity. In contrast, pro- and anti-inflammatory cytokines and chemokines can directly promote intracellular injury mechanisms by inducing nitric oxide synthase or inhibit cell death mechanisms by the expression of acute-phase proteins (HSPs, heme oxygenase-1) and promote hepatocyte proliferation. In addition, the newly recruited macrophages (M2) and potentially neutrophils are involved in the removal of necrotic cell debris in preparation for tissue repair and resolution of the inflammatory response. Thus, as discussed in detail in this review, the preponderance of experimental evidence suggests that the extensive sterile inflammatory response during APAP hepatotoxicity is predominantly beneficial by limiting the formation and the impact of pro-inflammatory mediators and by promoting tissue repair.
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What OpenQuestion holds
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.