ArticleLiver research (Beijing, China)2019
Mitochondrial Damage and Biogenesis in Acetaminophen-induced Liver Injury.
Article in Liver research (Beijing, China), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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Who cites it
31 citing papers in PubMed, 60 citations in OpenAlex.
- CPS1: a multipurpose mitochondrial enzyme, bile protein, acute liver injury biomarker, and cytokine.Gut · 2026Review
- TLR9-mediated innate immune signaling contributes to acetaminophen-induced injury in the developing lung.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Adipose-derived mesenchymal stem cell therapy modulates mitochondrial function to attenuate acetaminophen-induced liver injury by DDIT4/PGC-1α axis.Stem cell research & therapy · 2025Article
- Cryopreserved human alternatively activated macrophages promote resolution of acetaminophen-induced liver injury in mouse.NPJ Regenerative medicine · 2025Article
- Magnesium Isoglycyrrhizinate Alleviates Alectinib-Induced Hepatotoxicity by Inhibiting Mitochondrial Damage-Mediated Pyroptosis.Drug design, development and therapy · 2025Article
- Central Mechanisms of Acetaminophen Hepatotoxicity: Mitochondrial Dysfunction by Protein Adducts and Oxidant Stress.Drug metabolism and disposition: the biological fate of chemicals · 2024Review
- Unveiling the molecular basis of paracetamol-induced hepatotoxicity: Interaction ofBiochemistry and biophysics reports · 2024Article
- Larsucosterol: endogenous epigenetic regulator for treating chronic and acute liver diseases.American journal of physiology. Endocrinology and metabolism · 2024Review
- Gasdermin-E-Dependent Non-Canonical Pyroptosis Promotes Drug-Induced Liver Failure by Promoting CPS1 deISGylation and Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- Acetaminophen Hepatotoxicity: Paradigm for Understanding Mechanisms of Drug-Induced Liver Injury.Annual review of pathology · 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
- Development of KEAP1-targeting PROTAC and its antioxidant properties: In vitro and in vivo.Redox biology · 2023Article
- Article
- Intracellular Quantum Sensing of Free-Radical Generation Induced by Acetaminophen (APAP) in the Cytosol, in Mitochondria and the Nucleus of Macrophages.ACS sensors · 2022Article
- Targeting PARK7 Improves Acetaminophen-Induced Acute Liver Injury by Orchestrating Mitochondrial Quality Control and Metabolic Reprogramming.Antioxidants (Basel, Switzerland) · 2022Article
- Acetaminophen Hepatotoxicity: Not as Simple as One Might Think! Introductory Comments on the Special Issue-Livers · 2022Article
- Paracetamol preceding very preterm birth: Is it safe?Acta obstetricia et gynecologica Scandinavica · 2022Article
- Dual-Channel Fluorescent Probe for the Simultaneous Monitoring of Peroxynitrite and Adenosine-5'-triphosphate in Cellular Applications.Journal of the American Chemical Society · 2022Article
- Kupffer cells regulate liver recovery through induction of chemokine receptor CXCR2 on hepatocytes after acetaminophen overdose in mice.Archives of toxicology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Liver injury and acute liver failure caused by acetaminophen (APAP) overdose is the clinically most important drug toxicity in western countries. Mechanistic investigations have revealed a central role of mitochondria in the pathophysiology. Excess formation of the reactive metabolite N-acetyl-p-benzoquinone imine (NAPQI) after an overdose leads to hepatic glutathione depletion, mitochondrial protein adducts formation and an initial oxidant stress, which triggers the activation of mitogen activated protein (MAP) kinase cascade ultimately leading to c-jun N-terminal kinase (JNK) phosphorylation. Phospho-JNK translocates to the mitochondria and amplifies the oxidative and nitrosative stress eventually causing the mitochondrial membrane permeability transition pore opening and cessation of ATP synthesis. In addition, mitochondrial matrix swelling ruptures the outer membrane and releases endonucleases, which cause nuclear DNA fragmentation. Together, the nuclear DNA damage and the extensive mitochondrial dysfunction result in necrotic cell death. However, the pro-cell death signaling events are counteracted by adaptive responses such as autophagy and mitochondrial biogenesis. The improved mechanistic insight into the pathophysiology leads to better understanding of the mechanisms of action of the existing antidote N-acetylcysteine and justifies the clinical testing of novel therapeutics such as 4-methylpyrazole and calmangafodipir.
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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.