ReviewToxicology2017
Clinical effects of chemical exposures on mitochondrial function.
Review in Toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 70 citations in OpenAlex.
- Oxidative Stress-Mediated Mitochondrial Dysfunction Drives Genistein-Induced Apoptosis in TM4 Sertoli and ELT3 Leiomyoma Cells.Journal of xenobiotics · 2026Article
- Synergizing multimodal data and fingerprint space exploration for mechanism of action prediction.Bioinformatics (Oxford, England) · 2025Article
- High-Resolution Tracking of Aging-Related Small Molecules: Bridging Pollutant Exposure, Brain Aging Mechanisms, and Detection Innovations.Biosensors · 2025Review
- Mitochondrial Dysfunction and Risk Factors for Noncommunicable Diseases: From Basic Concepts to Future Prospective.Diseases (Basel, Switzerland) · 2024Review
- Air pollutants as modulators of mitochondrial quality control in cardiovascular disease.Physiological reports · 2024Review
- Neurotoxicity of Some Environmental Pollutants to Zebrafish.Life (Basel, Switzerland) · 2024Review
- Changing epidemiology of colorectal cancer - birth cohort effects and emerging risk factors.Nature reviews. Gastroenterology & hepatology · 2024Review
- Glutamine metabolism in diseases associated with mitochondrial dysfunction.Molecular and cellular neurosciences · 2023Review
- An Experimental Approach to Address the Functional Relationship between Antioxidant Enzymes and Mitochondrial Respiratory Complexes.Methods and protocols · 2023Article
- Raising the Alarm: Environmental Factors in the Onset and Maintenance of Chronic (Low-Grade) Inflammation in the Gastrointestinal Tract.Digestive diseases and sciences · 2022Review
- Arrhythmia prevalence and sudden death risk in adults with the m.3243A>G mitochondrial disorder.Open heart · 2022Article
- The Cause of Alzheimer's Disease: The Theory of Multipathology Convergence to Chronic Neuronal Stress.Aging and disease · 2022Article
- Neuronal Autophagy: Characteristic Features and Roles in Neuronal Pathophysiology.Biomolecules & therapeutics · 2021Review
- The Toxicity of Wiped Dust and Airborne Microbes in Individual Classrooms Increase the Risk of Teachers' Work-Related Symptoms: A Cross-Sectional Study.Pathogens (Basel, Switzerland) · 2021Article
- Review
- Utilization of Human Samples for Assessment of Mitochondrial Bioenergetics: Gold Standards, Limitations, and Future Perspectives.Life (Basel, Switzerland) · 2021Review
- MitoTox: a comprehensive mitochondrial toxicity database.BMC bioinformatics · 2021Article
- Reframing the Question: Does Mitochondrial Damage Set the Stage for Future Inflammation?Environmental health perspectives · 2021Article
- Flame Retardants-Mediated Interferon Signaling in the Pathogenesis of Nonalcoholic Fatty Liver Disease.International journal of molecular sciences · 2021Review
- Susceptibility to COVID-19 in populations with health disparities: Posited involvement of mitochondrial disorder, socioeconomic stress, and pollutants.Journal of biochemical and molecular toxicology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria are critical for the provision of ATP for cellular energy requirements. Tissue and organ functions are dependent on adequate ATP production, especially when energy demand is high. Mitochondria also play a role in a vast array of important biochemical pathways including apoptosis, generation and detoxification of reactive oxygen species, intracellular calcium regulation, steroid hormone and heme synthesis, and lipid metabolism. The complexity of mitochondrial structure and function facilitates its diverse roles but also enhances its vulnerability. Primary disorders of mitochondrial bioenergetics, or Primary Mitochondrial Diseases (PMD) are due to inherited genetic defects in the nuclear or mitochondrial genomes that result in defective oxidative phosphorylation capacity and cellular energy production. Secondary mitochondrial dysfunction is observed in a wide range of diseases such as Alzheimer's and Parkinson's disease. Several lines of evidence suggest that environmental exposures cause substantial mitochondrial dysfunction. Whereby literature from experimental and human studies on exposures associated with Alzheimer's and Parkinson's diseases exist, the significance of exposures as potential triggers in Primary Mitochondrial Disease (PMD) is an emerging clinical question that has not been systematically studied.
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.