ReviewToxicology2017
Mitochondria targeting by environmental stressors: Implications for redox cellular signaling.
Review in Toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 104 citations in OpenAlex.
- Transplantation of Ru265-treated mitochondria enhances the therapeutic impact on skeletal muscle ischemia-reperfusion injury.Molecular and cellular biochemistry · 2026Article
- Promoting Drp1-Mediated Mitochondrial Division in Nickel Nanoparticles-Induced Reproductive Toxicity in GC-2 Cells.Nanomaterials (Basel, Switzerland) · 2025Article
- Heavy metals: toxicity and human health effects.Archives of toxicology · 2025Review
- Air pollutants as modulators of mitochondrial quality control in cardiovascular disease.Physiological reports · 2024Review
- Vascular endothelial cells of Mongolian gerbils are resistant to cholesterol-induced mitochondrial dysfunction and oxidative damage.Experimental and therapeutic medicine · 2024Article
- Mechanisms Mediating the Combined Toxicity of Paraquat and Maneb in SH-SY5Y Neuroblastoma Cells.Chemical research in toxicology · 2024Article
- Liver and Pancreatic Toxicity of Endocrine-Disruptive Chemicals: Focus on Mitochondrial Dysfunction and Oxidative Stress.International journal of molecular sciences · 2024Review
- Redox mechanisms of environmental toxicants on male reproductive function.Frontiers in cell and developmental biology · 2024Review
- Exposome and unhealthy aging: environmental drivers from air pollution to occupational exposures.GeroScience · 2023Review
- The role of mitochondria in the peri-implant microenvironment.Experimental physiology · 2023Review
- Potential Roles of Metals in the Pathogenesis of Pulmonary and Systemic Hypertension.International journal of biological sciences · 2023Review
- Construction of the panoptosis-related gene model and characterization of tumor microenvironment infiltration in hepatocellular carcinoma.Oncology research · 2023Article
- Hepatotoxic mechanism of cantharidin: insights and strategies for therapeutic intervention.Frontiers in pharmacology · 2023Review
- Environmental Chemical Exposures and Mitochondrial Dysfunction: a Review of Recent Literature.Current environmental health reports · 2022Review
- Association between plasma level of superoxide dismutase and survival of patients with acute-on-chronic liver failure.BMC gastroenterology · 2022Article
- Serum superoxide dismutase level is a potential biomarker of disease prognosis in patients with HEV-induced liver failure.BMC gastroenterology · 2022Article
- From Mitochondria to Atherosclerosis: The Inflammation Path.Biomedicines · 2021Review
- Mitochondrial dysfunction resulting from the down-regulation of bone morphogenetic protein 5 may cause microtia.Annals of translational medicine · 2021Article
- MOLECULAR MECHANISMS OF LEAD NEUROTOXICITY.Advances in neurotoxicology · 2021Article
- Mitochondrial DNA 4977 bp Deletion in Peripheral Blood Is Associated With Polycystic Ovary Syndrome.Frontiers in endocrinology · 2021Article
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 2 institutions in 1 country.
Funding
Abstract
Mitochondria are cellular powerhouses as well as metabolic and signaling hubs regulating diverse cellular functions, from basic physiology to phenotypic fate determination. It is widely accepted that reactive oxygen species (ROS) generated in mitochondria participate in the regulation of cellular signaling, and that some mitochondria chronically operate at a high ROS baseline. However, it is not completely understood how mitochondria adapt to persistently high ROS states and to environmental stressors that disturb the redox balance. Here we will review some of the current concepts regarding how mitochondria resist oxidative damage, how they are replaced when excessive oxidative damage compromises function, and the effect of environmental toxicants (i.e. heavy metals) on the regulation of mitochondrial ROS (mtROS) production and subsequent impact.
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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.