ReviewJournal of clinical and translational research2018
Mitochondrial dysfunction as a mechanism of drug-induced hepatotoxicity: current understanding and future perspectives.
Review in Journal of clinical and translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 3 of them syntheses that pooled it.
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
86 citing papers in PubMed, 3 syntheses or guidelines pooled it, 178 citations in OpenAlex.
- Genetic polymorphisms and anti-tuberculosis drug-induced liver injury: an umbrella review of the evidence.International journal of clinical pharmacy · 2025Pooled it
- Efficacy, safety, and pharmacokinetics of isoniazid affected by NAT2 polymorphisms in patients with tuberculosis: A systematic review.Clinical and translational science · 2024Pooled it
- NR1I2 genetic polymorphisms and the risk of anti-tuberculosis drug-induced hepatotoxicity: A systematic review and meta-analysis.Pharmacology research & perspectives · 2020Pooled it
- Mitochondrial quality control in acute liver injury and its therapeutic implications (Review).Molecular medicine reports · 2026Review
- Article
- Fasudil Protects Against Diclofenac-Induced Hepatorenal and Gastric Injury via Modulation of ROCK/TLR4/SIRT1 Signaling and Preservation of Tight Junctions.Journal of xenobiotics · 2026Article
- Article
- Construction of liver organoid models by hepatobiliary differentiation from human induced pluripotent stem cells: state of the art, challenges and improving strategies.Stem cell research & therapy · 2026Review
- Network pharmacology and molecular modelling analysis ofFrontiers in bioinformatics · 2026Article
- Oridonin attenuates diclofenac-induced organ damage by suppressing endoplasmic reticulum stress and inflammasome activation.Frontiers in toxicology · 2026Article
- Mitochondrial DNA variants and susceptibility to anti-tuberculosis drug-induced liver injury in Korean patients.The pharmacogenomics journal · 2025Article
- Article
- PANoptosis-mediated mechanisms underlying AST elevation in Talaromyces marneffei infection.PLoS neglected tropical diseases · 2025Article
- In vitro investigation of the toxicological mechanisms of Fingolimod (S)-phosphate in HEPG2 cells.Toxicology research · 2025Article
- Drug-Induced Liver Injury: Mechanisms, Diagnosis, and Management: A Review.Journal of pharmacy & bioallied sciences · 2025Review
- Chronic Exposure to Arsenic and Fluoride Starting at Gestation Alters Liver Mitochondrial Protein Expression and Induces Early Onset of Liver Fibrosis in Male Mouse Offspring.Biological trace element research · 2025Article
- Deep Learning Prediction of Drug-Induced Liver Toxicity by Manifold Embedding of Quantum Information of Drug Molecules.Pharmaceutical research · 2025Article
- Ferroptosis and Intrinsic Drug-induced Liver Injury by Acetaminophen and Other Drugs: A Critical Evaluation and Historical Perspective.Journal of clinical and translational hepatology · 2024Review
- Article
- Drug-induced oxidative stress actively prevents caspase activation and hepatocyte apoptosis.Cell death & disease · 2024Article
26 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
5 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria are critical cellular organelles for energy generation and are now also recognized as playing important roles in cellular signaling. Their central role in energy metabolism, as well as their high abundance in hepatocytes, make them important targets for drug-induced hepatotoxicity. This review summarizes the current mechanistic understanding of the role of mitochondria in drug-induced hepatotoxicity caused by acetaminophen, diclofenac, anti-tuberculosis drugs such as rifampin and isoniazid, anti-epileptic drugs such as valproic acid and constituents of herbal supplements such as pyrrolizidine alkaloids. The utilization of circulating mitochondrial-specific biomarkers in understanding mechanisms of toxicity in humans will also be examined. In summary, it is well-established that mitochondria are central to acetaminophen-induced cell death. However, the most promising areas for clinically useful therapeutic interventions after acetaminophen toxicity may involve the promotion of adaptive responses and repair processes including mitophagy and mitochondrial biogenesis, In contrast, the limited understanding of the role of mitochondria in various aspects of hepatotoxicity by most other drugs and herbs requires more detailed mechanistic investigations in both animals and humans. Development of clinically relevant animal models and more translational studies using mechanistic biomarkers are critical for progress in this area.
Indexed as
Identifiers
30873497PMC6261533W2807488747What 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.