ReviewExpert opinion on drug metabolism & toxicology2015
Pathophysiological significance of c-jun N-terminal kinase in acetaminophen hepatotoxicity.
Review in Expert opinion on drug metabolism & toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 65 citations in OpenAlex.
- Binankadsurin A fromNutrients · 2026Article
- Advances in drug-induced liver injury research: in vitro models, mechanisms, omics and gene modulation techniques.Cell & bioscience · 2024Review
- Hepatocyte-specific deletion of small heterodimer partner protects mice against acetaminophen-induced hepatotoxicity via activation of Nrf2.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- Inhibitor of nuclear factor kappa B kinase subunit epsilon regulates murine acetaminophen toxicity via RIPK1/JNK.Cell biology and toxicology · 2023Article
- Review
- Activation of the adenosine A2B receptor even beyond the therapeutic window of N-acetylcysteine accelerates liver recovery after an acetaminophen overdose.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2022Article
- Mitochondria as the Target of Hepatotoxicity and Drug-Induced Liver Injury: Molecular Mechanisms and Detection Methods.International journal of molecular sciences · 2022Review
- Extracellular vesicles: Roles and applications in drug-induced liver injury.Advances in clinical chemistry · 2021Review
- The development and hepatotoxicity of acetaminophen: reviewing over a century of progress.Drug metabolism reviews · 2020Review
- Novel Therapeutic Approaches Against Acetaminophen-induced Liver Injury and Acute Liver Failure.Toxicological sciences : an official journal of the Society of Toxicology · 2020Review
- Effects of Photoperiod on Acetaminophen-Induced Hepatotoxicity in Mice.Digestive diseases and sciences · 2020Article
- Expression of mitochondrial membrane-linked SAB determines severity of sex-dependent acute liver injury.The Journal of clinical investigation · 2019Article
- Mitochondrial Damage and Biogenesis in Acetaminophen-induced Liver Injury.Liver research (Beijing, China) · 2019Article
- Emerging and established modes of cell death during acetaminophen-induced liver injury.Archives of toxicology · 2019Review
- Design and synthesis of acetaminophen probe APAP-P1 for identification of the toxicity targets thioredoxin reductase-1 in HepaRG cells.RSC advances · 2019Article
- Animal models of drug-induced liver injury.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- Chlorpromazine protects against acetaminophen-induced liver injury in mice by modulating autophagy and c-Jun N-terminal kinase activation.Liver research (Beijing, China) · 2019Article
- Mechanisms and biomarkers of liver regeneration after drug-induced liver injury.Advances in pharmacology (San Diego, Calif.) · 2019Review
- 4-Methylpyrazole protects against acetaminophen hepatotoxicity in mice and in primary human hepatocytes.Human & experimental toxicology · 2018Article
- Therapeutic Potential of Plants and Plant Derived Phytochemicals against Acetaminophen-Induced Liver Injury.International journal of molecular sciences · 2018Review
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
backgroundAcetaminophen (APAP) overdose is the leading cause of acute liver failure in the US. Although substantial progress regarding the mechanisms of APAP hepatotoxicity has been made in the past several decades, therapeutic options are still limited and novel treatments are clearly needed. c-jun N-terminal Kinase (JNK) has emerged as a promising therapeutic target in recent years. AREAS COVERED: Early studies established the critical role of JNK activation and mitochondrial translocation in APAP hepatotoxicity. However, this concept has also been challenged. Initial studies failed to reproduce the protection of JNK deficiency in APAP toxicity and concerns over off-target effects of JNK inhibitors and even in knock-out mice are increasing. Interestingly, recent studies have even shown that liver injury can be altered with or without effects on JNK activation. The current review addresses these discrepancies and tries to explain or reconcile some of the conflicting results. EXPERT OPINION: JNK is a potential therapeutic target for APAP poisoning. However, controversies still exist regarding its actual role in APAP hepatotoxicity. Future studies are warranted for more in-depth testing of specific inhibitors in well-defined preclinical models and human hepatocytes before JNK can be considered a relevant therapeutic target for APAP poisoning.
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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.