ReviewThe American journal of pathology2019
Liver Regeneration after Acetaminophen Hepatotoxicity: Mechanisms and Therapeutic Opportunities.
Review in The American journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
107 citing papers in PubMed, 169 citations in OpenAlex.
- Article
- MSCs overexpressing FGF21 alleviate acetaminophen-induced acute liver injury by eliciting macrophage-mediated phagocytosis.Hepatology communications · 2026Article
- Progranulin drives acetaminophen-induced acute liver injury by limiting hepatic recruitment of eosinophilsActa pharmaceutica Sinica. B · 2026Article
- Immunoglobulin κ drives liver regeneration by stabilizing MYLK to maintain cytoskeletal integrity and promote hepatocyte proliferation.Journal of translational internal medicine · 2026Article
- Preoperative Beta-Hydroxy-Beta-Methyl-Butyrate Supplementation Reduces Mitochondrial Dynamics Proteins and Preserves Hepatic Mitochondrial Function After Partial Hepatectomy in Mice.Acta physiologica (Oxford, England) · 2026Article
- Acute-on-chronic liver failure: pathophysiological mechanisms and clinical management.Nature reviews. Gastroenterology & hepatology · 2026Review
- Oxidative Stress and Antioxidant Defense During Liver Regeneration After Acetaminophen Toxicity: The Preventive Potential of the MicroalgaAntioxidants (Basel, Switzerland) · 2026Article
- Gallium-Doped MXene Nanozymes Protect Liver Through Multi-Death Pathway Blockade and Hepatocyte Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Hepatocyte-Specific MET Deletion Exacerbates Acetaminophen-Induced Hepatotoxicity in Mice.The American journal of pathology · 2026Article
- Hepatocyte-specific epidermal growth factor receptor (EGFR) deletion attenuates acetaminophen-induced liver injury in mice.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Modeling Metabolite Kinetics with a Partial Differential Equation-Based Hepatic Sinusoidal Model and MALDI-Mass Spectrometry Imaging of Verapamil and Its Metabolites.Journal of medicinal chemistry · 2026Article
- Risk factors for irinotecan-induced hepatotoxicity: a retrospective cohort study.Frontiers in oncology · 2026Article
- Crosstalk along the gut-liver axis modulates glutathione and cadmium-induced hepatotoxicity.Frontiers in immunology · 2026Review
- Article
- CpG-oligodeoxynucleotides challenged macrophages ameliorate acetaminophen induced liver injury by activating TLR9/IRG1/itaconate metabolic pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- Glucocorticoids trigger muscle-liver crosstalk to attenuate acute liver injury and promote liver regeneration via the FGF6-FGFBP1 axis.Military Medical Research · 2025Article
- IL-37 ameliorates acetaminophen-induced acute liver injury by limiting MAPK/NFκB signaling-mediated liver inflammation.Scientific reports · 2025Article
- Acetaminophen, a new tool for the refinement of the experimental infection of toxoplasmosis in mice.Scientific reports · 2025Article
- Neuronal activation in the axolotl brain promotes tail regeneration.NPJ Regenerative medicine · 2025Article
- Role of mitogens in normal and pathological liver regeneration.Hepatology communications · 2025Review
47 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
Acetaminophen (N-acetyl-para-aminophenol; APAP) overdose is the most common cause of acute liver failure in the Western world, with limited treatment opportunities. For years, research on APAP overdose has been focused on investigating the mechanisms of hepatotoxicity, with limited success in advancing therapeutic strategies. Acute liver injury after any insult, including APAP overdose, is followed by compensatory liver regeneration, which promotes recovery and is a crucial determinant of the final outcome. Liver regeneration after APAP-induced liver injury is dose dependent and impaired after severe APAP overdose. Although robust regenerative response is associated with spontaneous recovery and survival, impaired regeneration results in faster progression of injury and death after APAP overdose. APAP hepatotoxicity-induced liver regeneration involves a complex time- and dose-dependent interplay of several signaling mediators, including growth factors, cytokines, angiogenic factors, and other mitogenic pathways. Compared with the liver injury, which is established before most patients seek medical attention and has proved difficult to manipulate, liver regeneration can be potentially modulated even in late-stage APAP-induced acute liver failure. Despite recent efforts to study the mechanisms of liver regeneration after APAP-induced liver injury, more comprehensive research in this area is required, especially regarding factors that contribute to impaired regenerative response, to develop novel regenerative therapies for APAP-induced acute liver failure.
Indexed as
Identifiers
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.