ReviewFrontiers in physiology2017
Role of Mitochondrial Reverse Electron Transport in ROS Signaling: Potential Roles in Health and Disease.
Review in Frontiers in physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 289 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
289 citing papers in PubMed, 481 citations in OpenAlex.
- PolyQ-expanded ataxin-3 is associated with mitochondrial alterations in Machado-Joseph disease.Disease models & mechanisms · 2026Article
- Mitochondrial complex I as a master regulator of redox signaling: From structural architecture to directionality of electron transport.Free radical biology & medicine · 2026Review
- Metformin Attenuates Sepsis-Induced Cardiomyopathy via Inhibition of Reverse Electron Transfer at Mitochondrial Complex I.Biology · 2026Article
- Oxaloacetate inhibition of succinate dehydrogenase: mechanism and physiological implications.American journal of physiology. Cell physiology · 2026Review
- A Function-Centric Framework for Mitochondrial Quality Control.Biomolecules · 2026Review
- Plant-derived mitochondria mitigate aging-related neurodegeneration by reprogramming microglial mitochondrial energy metabolism.Translational neurodegeneration · 2026Article
- Review
- Mitophagy in Hepatic Ischemia-Reperfusion Injury: From Mitochondrial Dysfunction to Therapeutic Targeting.Biomolecules · 2026Review
- Neoagarotetraose from Marine Red Algae Attenuates Hypertensive Vascular Remodeling by Targeting FoxO4 to Inhibit Mitochondrial Superoxide Generation.Journal of agricultural and food chemistry · 2026Article
- Tuning the Fire: Context-Dependent Mitochondrial ROS Signaling, Mitohormesis, and Redox-Modulating Interventions.Biomolecules · 2026Review
- Reply to Lemieux et al.: Integration does not preclude essentiality of mitochondrial glycerol-3-phosphate dehydrogenase.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- CoQExperimental & molecular medicine · 2026Review
- Hypoxia/Reoxygenation-Induced Mitochondrial Reverse Electron Transfer: A Targetable Mechanism to Enhance Radiosensitivity in Non-Small Cell Lung Cancer.Antioxidants (Basel, Switzerland) · 2026Article
- Review
- Small extracellular vesicle signaling and mitochondrial transfer reprogram T helper cell function in human asthma.Nature communications · 2026Article
- EndMT in vascular cognitive impairment and dementia: mechanisms, evidence gaps, and therapeutic opportunities.Molecular medicine (Cambridge, Mass.) · 2026Review
- Cryptic DNA sequences encode a temperature sensor to regulate mitochondrial suicide during neuronal differentiation.Cell communication and signaling : CCS · 2026Article
- Quantum biology: From mechanisms to medicine.Clinical and translational medicine · 2026Review
- Differential Effects of 825 nm and 525 nm Photobiomodulation on Neural Differentiation and Mitochondrial Activity in ADSC-Derived Neurospheres.ACS chemical neuroscience · 2026Article
- The role and therapeutic potential of succinate and succinylation in cardiovascular diseases.Clinical epigenetics · 2026Review
229 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 at 2 institutions in 2 countries.
Funding
Abstract
Reactive Oxygen Species (ROS) can cause oxidative damage and have been proposed to be the main cause of aging and age-related diseases including cancer, diabetes and Parkinson's disease. Accordingly, mitochondria from old individuals have higher levels of ROS. However, ROS also participate in cellular signaling, are instrumental for several physiological processes and boosting ROS levels in model organisms extends lifespan. The current consensus is that low levels of ROS are beneficial, facilitating adaptation to stress via signaling, whereas high levels of ROS are deleterious because they trigger oxidative stress. Based on this model the amount of ROS should determine the physiological effect. However, recent data suggests that the site at which ROS are generated is also instrumental in determining effects on cellular homeostasis. The best example of site-specific ROS signaling is reverse electron transport (RET). RET is produced when electrons from ubiquinol are transferred back to respiratory complex I, reducing NAD+ to NADH. This process generates a significant amount of ROS. RET has been shown to be instrumental for the activation of macrophages in response to bacterial infection, re-organization of the electron transport chain in response to changes in energy supply and adaptation of the carotid body to changes in oxygen levels. In
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.