ReviewAntioxidants (Basel, Switzerland)2019
Physiologic Implications of Reactive Oxygen Species Production by Mitochondrial Complex I Reverse Electron Transport.
Review in Antioxidants (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed.
- Molecular insights into the response of Acidithiobacillus caldus to leached metal toxicity during bioleaching of spent FCC catalyst.Extremophiles : life under extreme conditions · 2026Article
- Article
- Redox-modulation of regulated cell death: implications for synergistic anticancer therapies.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Tuning the Fire: Context-Dependent Mitochondrial ROS Signaling, Mitohormesis, and Redox-Modulating Interventions.Biomolecules · 2026Review
- Mitochondrial dysfunction underlies cardiac contractility and growth defects in a zebrafish model ofbioRxiv : the preprint server for biology · 2026Article
- Moonlighting cytosolic function of ACAD9: suppression of TRAF6-mediated osteoclastogenesis and protection against osteoporosis.Cell death & disease · 2026Article
- Mitochondrial ROS in Retinal Neurodegeneration: Thresholds, Quality Control Failure, and Precision Therapeutic Windows.Biomolecules · 2026Review
- Understanding molecular mechanisms driving cadmium-induced mitochondrial dysfunction in human metabolic liver disease.Environmental toxicology and pharmacology · 2026Review
- A genetic screen for modifiers of cohesin clustering identifies regulators of genome folding.Science advances · 2026Article
- Simultaneous sulfide oxidation and sulfate reduction for intracellular redox homeostasis under highly acidic conditions.Nature communications · 2026Article
- Roles of mitochondrial complexes in non-alcoholic fatty liver disease.Frontiers in molecular biosciences · 2026Review
- Sex dimorphism and substrate dependency of liver mitochondrial bioenergetics and HAmerican journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Mitochondrial reactive oxygen species production in lungs of rats with different susceptibilities to hyperoxia-induced acute lung injury.Biochimica et biophysica acta. Bioenergetics · 2025Article
- Mitochondrial uncoupling, energy substrate utilization, and brown adipose tissue as therapeutic targets in cancer.npj metabolic health and disease · 2025Review
- Complex Interplay of Metabolic Substrates, Points of Entry into the Mitochondrial Electron Chain, and ROS Generation: A critical analysis of "Active control of mitochondrial network morphology by metabolism-driven redox state" by Singh et al. and studies replacing ETC components with yeast counterparts.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- The Role of ROS-Mediated Mitochondrial Dysfunction in the Development of Malignant Melanoma.Experimental dermatology · 2025Review
- Oxidative stress in cancer: from tumor and microenvironment remodeling to therapeutic frontiers.Molecular cancer · 2025Review
- Oxidative Stress in the Pathophysiology of Chronic Venous Disease: An Overview.Antioxidants (Basel, Switzerland) · 2025Review
- Mitochondrial Metabolomics in Cancer: Mass Spectrometry-Based Approaches for Metabolic Rewiring Analysis and Therapeutic Discovery.Metabolites · 2025Review
- Coenzyme Q10 and Xenobiotic Metabolism: An Overview.International journal of molecular sciences · 2025Review
7 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
3 authors.
Funding
Abstract
Mitochondrial reactive oxygen species (ROS) can be either detrimental or beneficial depending on the amount, duration, and location of their production. Mitochondrial complex I is a component of the electron transport chain and transfers electrons from NADH to ubiquinone. Complex I is also a source of ROS production. Under certain thermodynamic conditions, electron transfer can reverse direction and reduce oxygen at complex I to generate ROS. Conditions that favor this reverse electron transport (RET) include highly reduced ubiquinone pools, high mitochondrial membrane potential, and accumulated metabolic substrates. Historically, complex I RET was associated with pathological conditions, causing oxidative stress. However, recent evidence suggests that ROS generation by complex I RET contributes to signaling events in cells and organisms. Collectively, these studies demonstrate that the impact of complex I RET, either beneficial or detrimental, can be determined by the timing and quantity of ROS production. In this article we review the role of site-specific ROS production at complex I in the contexts of pathology and physiologic signaling.
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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.