ReviewDrug safety2016
Drug-Induced Mitochondrial Toxicity.
Review in Drug safety, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis 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
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Safety of drug use in patients with a primary mitochondrial disease: An international Delphi-based consensus.Journal of inherited metabolic disease · 2020Guideline
- Trial
- Animal models accurately representing acute liver failure (Review).International journal of molecular medicine · 2026Review
- Sodium formate-induced mitochondrial impairment and cytotoxicity in neuronal cells reveal crucial pathogenic mechanisms underlying diabetic neuropathy and retinopathy.Scientific reports · 2025Article
- The Effect of the Antidepressant Citalopram on the Bioconcentration and Biomarker Response ofToxics · 2025Article
- Direct exposure with exogenous mitochondria reduce colistin-induced mitochondrial dysfunction and cellular damages in isolated rat renal proximal tubular cells.Journal of molecular histology · 2025Article
- Therapeutic Approach to Epilepsy in Patients with Mitochondrial Diseases.Yonsei medical journal · 2025Review
- Attention-based deep learning for accurate cell image analysis.Scientific reports · 2025Article
- Application of a fully 3D printed carbon electrode for the double potential step Chronoamperometric determination of 2,4-dinitrophenol in environmental water samples.Frontiers in chemistry · 2025Article
- New insights into the nutritional genomics of adult-onset riboflavin-responsive diseases.Nutrition & metabolism · 2023Review
- Drug-induced mitochondrial toxicity: Risks of developing glucose handling impairments.Frontiers in endocrinology · 2023Review
- Remarks on Mitochondrial Myopathies.International journal of molecular sciences · 2022Review
- Mitochondrial Effects of Common Cardiovascular Medications: The Good, the Bad and the Mixed.International journal of molecular sciences · 2022Review
- The Potential ofCells · 2022Review
- Review
- Analysis of Mitochondrial Function in Cell Membranes as Indicator of Tissue Vulnerability to Drugs in Humans.Biomedicines · 2022Article
- Article
- Disease Modeling of Mitochondrial Cardiomyopathy Using Patient-Specific Induced Pluripotent Stem Cells.Biology · 2021Review
- Treatment with the direct oral anticoagulants (DOACs) apixaban and rivaroxaban associated with significant worsening of behavioural and psychological symptoms of dementia (BPSD).BMJ case reports · 2021Article
- Diet aid or aid to die: an update on 2,4-dinitrophenol (2,4-DNP) use as a weight-loss product.Archives of toxicology · 2020Review
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 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mitochondrial respiratory chain (MRC) and ATP synthase (complex V) play an essential role in cellular energy production by the process of oxidative phosphorylation. In addition to inborn errors of metabolism, as well as secondary causes from disease pathophysiology, an impairment of oxidative phosphorylation can result from drug toxicity. These 'off-target' pharmacological effects can occur from a direct inhibition of MRC enzyme activity, an induction of mitochondrial oxidative stress, an uncoupling of oxidative phosphorylation, an impairment of mitochondrial membrane structure or a disruption in the replication of mitochondrial DNA. The purpose of this review is to focus on the off-target mitochondrial toxicity associated with both commonly used pharmacotherapies and a topical 'weight loss' agent. The mechanisms of drug-induced mitochondrial impairment will be discussed together with putative therapeutic strategies to counteract the adverse effects of the pharmacotherapy.
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.