ReviewAdvances in pharmacology (San Diego, Calif.)2019
Acetaminophen hepatotoxicity: A mitochondrial perspective.
Review in Advances in pharmacology (San Diego, Calif.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed.
- HarnessingFood science & nutrition · 2026Review
- A systems pharmacology model for paracetamol overdose and treatment.Journal of pharmacokinetics and pharmacodynamics · 2026Article
- Article
- Membrane-Targeted Consequences of Acetaminophen Toxicity and Off-Target Effects of Antimicrobial Peptides on Host Cell Membranes.International journal of molecular sciences · 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
- Metabolomics and Network Pharmacology-Based Screening of Candidate Hepatoprotective Metabolites in FermentedCurrent issues in molecular biology · 2026Article
- The zebrafish model: a versatile platform for uncovering the therapeutic potential of phytochemicals in liver diseases.Frontiers in pharmacology · 2026Review
- Subchronic Alcohol Exposure Exacerbates Acetaminophen-Induced Acute Liver Injury via Macrophage-Mediated Inflammation and Mitochondrial Dysfunction.Mediators of inflammation · 2026Article
- Betaine-homocysteine methyltransferase protects against acetaminophen-induced acute liver failure via BACH1-SCD1-oleic acid axis.Acta pharmacologica Sinica · 2026Article
- Developmentally Regulated CYP2E1 Expression Is Associated with a Fetal Pulmonary Transcriptional Response to Maternal Acetaminophen Exposure.Biomedicines · 2025Article
- A Single Early-Life Acetaminophen Exposure Causes Persistent Abnormalities in the Murine Lung.American journal of respiratory cell and molecular biology · 2025Article
- NLRP3 inflammasome: structure, mechanism, drug-induced organ toxicity, therapeutic strategies, and future perspectives.RSC medicinal chemistry · 2025Review
- Yijing Decoction improves premature ovarian failure in rats by activating VEGF/VEGFR-2/FAK pathway.Journal of ovarian research · 2025Article
- Gardenia jasminoides extract mitigates acetaminophen-induced liver damage in mice.BMC complementary medicine and therapies · 2024Article
- Drug-induced oxidative stress actively prevents caspase activation and hepatocyte apoptosis.Cell death & disease · 2024Article
- Article
- Neutrophil extracellular traps promote acetaminophen-induced acute liver injury in mice via AIM2.Acta pharmacologica Sinica · 2024Article
- Central Mechanisms of Acetaminophen Hepatotoxicity: Mitochondrial Dysfunction by Protein Adducts and Oxidant Stress.Drug metabolism and disposition: the biological fate of chemicals · 2024Review
- Article
- Contributing roles of mitochondrial dysfunction and hepatocyte apoptosis in liver diseases through oxidative stress, post-translational modifications, inflammation, and intestinal barrier dysfunction.Cellular and molecular life sciences : CMLS · 2024Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Acetaminophen (APAP) is a highly effective analgesic, which is safe at therapeutic doses. However, an overdose can cause hepatotoxicity and even liver failure. APAP toxicity is currently the most common cause of acute liver failure in the United States. Decades of research on mechanisms of liver injury have established the role of mitochondria as central players in APAP-induced hepatocyte necrosis and this chapter examines the various facets of the organelle's involvement in the process of injury as well as in resolution of damage. The injury process is initiated by formation of a reactive metabolite, which binds to sulfhydryl groups of cellular proteins including mitochondrial proteins. This inhibits the electron transport chain and leads to formation of reactive oxygen species, which induce the activation of redox-sensitive members of the MAP kinase family ultimately causing activation of c-Jun N terminal kinase, JNK. Translocation of JNK to the mitochondria then amplifies mitochondrial dysfunction, ultimately resulting in mitochondrial permeability transition and release of mitochondrial intermembrane proteins, which trigger nuclear DNA fragmentation. Together, these events result in hepatocyte necrosis, while adaptive mechanisms such as mitophagy remove damaged mitochondria and minimize the extent of the injury. This oscillation between recovery and necrosis is predominant in cells at the edge of the necrotic area in the liver, where induction of mitochondrial biogenesis is important for liver regeneration. All these aspects of mitochondria in APAP hepatotoxicity, as well as their relevance to humans with APAP overdose and development of therapeutic approaches will be examined in detail in this chapter.
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