ReviewAntioxidants (Basel, Switzerland)2023
Reverse Electron Transport at Mitochondrial Complex I in Ischemic Stroke, Aging, and Age-Related Diseases.
Review in Antioxidants (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 43 citations in OpenAlex.
- The Reductive Stress Nexus: Integrated Pathways of Metabolic Dysregulation, Senescence and Blood-Brain Barrier Failure in Neurodegenerative Disease and Brain Aging.Cell biochemistry and biophysics · 2026Review
- Article
- Mitochondrial reactive oxygen species regulate HIF-1α stabilization and methylglyoxal accumulation in classically activated mouse macrophages.Immunometabolism (Cobham, Surrey) · 2026Review
- Astrocytic Mitochondria Transplantation Rescues Neuron Loss and Dendritic Injuries in Acute Cerebral Ischemic Stroke Mouse Model by Flexibly Regulating Mitochondria Dynamics.Annals of neurology · 2026Article
- CoQExperimental & molecular medicine · 2026Review
- Unravelling Mechanisms of Oxinflammation Induced by Heavy Metals.Metabolites · 2026Review
- Necrosis by sodium overload: a potential mechanism for renal diseases associated with mitochondrial dysfunction.Cell death discovery · 2026Article
- Mitochondrial Dysfunction in the Inflammatory Process of Neurodegenerative Diseases.Biomedicines · 2026Review
- Cerebral Ischemia-Reperfusion Injury: Unraveling the Mitophagy-Oxidative Stress Axis for Neuroprotective Strategies.International journal of molecular sciences · 2026Review
- Antidepressant Effects of L-Arginine and Its Role in Brain Energy MetabolismIranian biomedical journal · 2026Article
- Hub genes and diagnostic model associated with mitochondrial function in Alzheimer's disease.Animal models and experimental medicine · 2026Article
- Article
- Piperine improves ischemic brain injury by promoting the regulation of the AMPK/PGC-1α pathway by Apelin 13.Frontiers in pharmacology · 2026Article
- Integrative network toxicology, transcriptomic, and molecular docking approaches to elucidate the toxicity and mechanisms of bisphenol A in stroke.BMC pharmacology & toxicology · 2025Article
- NEK7 couples SDHB to orchestrate respiratory chain electron transport homeostasis that impedes liver fibrosis.Nature communications · 2025Article
- From Electron Imbalance to Network Collapse: Decoding the Redox Code of Ischemic Stroke for Biomarker-Guided Precision Neuroprotection.International journal of molecular sciences · 2025Review
- Reperfusion stroke injury and brain atrophy: a penumbra of progressive cognitive decline.Annals of medicine and surgery (2012) · 2025Article
- Harnessing Mitochondrial Function for Post-Stroke Rehabilitation: Unlocking Antioxidant Power.Antioxidants (Basel, Switzerland) · 2025Review
- Total ginsenosides and ginsenoside Rb2 delay hepatocyte senescence by regulating NADJournal of ginseng research · 2025Article
- Succinate Dehydrogenase Subunit A (SDHA) Mediated Microglia Extracellular Traps Formation Participating in Cerebral Ischemic Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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
Stroke is one of the leading causes of morbidity and mortality worldwide. A main cause of brain damage by stroke is ischemia-reperfusion (IR) injury due to the increased production of reactive oxygen species (ROS) and energy failure caused by changes in mitochondrial metabolism. Ischemia causes a build-up of succinate in tissues and changes in the mitochondrial NADH: ubiquinone oxidoreductase (complex I) activity that promote reverse electron transfer (RET), in which a portion of the electrons derived from succinate are redirected from ubiquinol along complex I to reach the NADH dehydrogenase module of complex I, where matrix NAD
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.