ReviewJournal of neuroscience research
Pyruvate dehydrogenase complex: metabolic link to ischemic brain injury and target of oxidative stress.
Review in Journal of neuroscience research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
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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.
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Who cites it
75 citing papers in PubMed, 168 citations in OpenAlex.
- Mitochondrial dysfunction in PTSD: A mechanism to understand trauma susceptibility?Psychopharmacology · 2026Review
- Gut microbiota dysbiosis and metabolic reprogramming in pediatric migraine: a multi-omics analysis revealing diagnostic biomarkers.The journal of headache and pain · 2026Article
- KAT2B regulates estradiol synthesis via H3K27ac/PPARα in granulosa cells of PCOS patients.Journal of translational medicine · 2025Article
- Genetically encoded biosensors of metabolic function for the study of neurodegeneration, a review and perspective.Neurophotonics · 2025Review
- Multi-target-directed therapeutic strategies for Alzheimer's disease: controlling amyloid-β aggregation, metal ion homeostasis, and enzyme inhibition.Chemical science · 2025Review
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- Article
- Metabolic aspects of genetic ion channel epilepsies.Journal of neurochemistry · 2024Review
- Altered Energy Metabolism, Mitochondrial Dysfunction, and Redox Imbalance Influencing Reproductive Performance in Granulosa Cells and Oocyte During Aging.Reproductive sciences (Thousand Oaks, Calif.) · 2024Review
- Pyruvate Dehydrogenase Complex in Neonatal Hypoxic-Ischemic Brain Injury.ACS pharmacology & translational science · 2024Review
- Glucose metabolic reprogramming-related parameters for the prediction of 28-day neurological prognosis and all-cause mortality in patients after cardiac arrest: a prospective single-center observational study.World journal of emergency medicine · 2024Article
- Phenylbutyrate and Dichloroacetate Enhance the Liquid-Stored Boar Sperm Quality via PDK1 and PDK3.International journal of molecular sciences · 2023Article
- Clinical targeting of the cerebral oxygen cascade to improve brain oxygenation in patients with hypoxic-ischaemic brain injury after cardiac arrest.Intensive care medicine · 2023Review
- Neuroprotective Effects and Therapeutic Potential of Dichloroacetate: Targeting Metabolic Disorders in Nervous System Diseases.International journal of nanomedicine · 2023Review
- Combined Treatment of Dichloroacetic Acid and Pyruvate Increased Neuronal Survival after Seizure.Nutrients · 2022Article
- Mechanistic Effects of Baicalein on Aqueous Humor Drainage and Intraocular Pressure.International journal of molecular sciences · 2022Article
- Exogenous Ketones and Lactate as a Potential Therapeutic Intervention for Brain Injury and Neurodegenerative Conditions.Frontiers in human neuroscience · 2022Review
- A Novel Therapeutic Approach With Sodium Pyruvate on Vital Signs, Acid-Base, and Metabolic Disturbances in Rats With a Combined Blast and Hemorrhagic Shock.Frontiers in neurology · 2022Article
- Neuroprotective Strategies in Aneurysmal Subarachnoid Hemorrhage (aSAH).International journal of molecular sciences · 2021Review
- Mitochondria-Targeted Therapeutics for Alzheimer's Disease: The Good, the Bad, the Potential.Antioxidants & redox signaling · 2021Review
15 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 1 institution in 1 country.
Funding
Abstract
The mammalian pyruvate dehydrogenase complex (PDHC) is a mitochondrial matrix enzyme complex (greater than 7 million Daltons) that catalyzes the oxidative decarboxylation of pyruvate to form acetyl CoA, nicotinamide adenine dinucleotide (the reduced form, NADH), and CO(2). This reaction constitutes the bridge between anaerobic and aerobic cerebral energy metabolism. PDHC enzyme activity and immunoreactivity are lost in selectively vulnerable neurons after cerebral ischemia and reperfusion. Evidence from experiments carried out in vitro suggests that reperfusion-dependent loss of activity is caused by oxidative protein modifications. Impaired enzyme activity may explain the reduced cerebral glucose and oxygen consumption that occurs after cerebral ischemia. This hypothesis is supported by the hyperoxidation of mitochondrial electron transport chain components and NAD(H) that occurs during reperfusion, indicating that NADH production, rather than utilization, is rate limiting. Additional support comes from the findings that immediate postischemic administration of acetyl-L-carnitine both reduces brain lactate/pyruvate ratios and improves neurologic outcome after cardiac arrest in animals. As acetyl-L-carnitine is converted to acetyl CoA, the product of the PDHC reaction, it follows that impaired production of NADH is due to reduced activity of either PDHC or one or more steps in glycolysis. Impaired cerebral energy metabolism and PDHC activity are associated also with neurodegenerative disorders including Alzheimer's disease and Wernicke-Korsakoff syndrome, suggesting that this enzyme is an important link in the pathophysiology of both acute brain injury and chronic neurodegeneration.
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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.