ReviewBrain sciences2020
Role of NAD
Review in Brain sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 18 citations in OpenAlex.
- Post-Translational Modifications in Traumatic Brain Injury: Decoding the Proteomic Landscape and Molecular Mechanisms of Secondary Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Maternal metabolic stress regulates progeny intestinal stem cell niche signaling through heritable changes in redox metabolites.Nature communications · 2026Article
- Pentose Phosphate Pathway Is Critical for Providing Energy by Bypassing 6-Phosphofructo-1-Kinase (PFK1) During Increased Neuronal Activity.Metabolites · 2026Review
- Mechanisms Linking Obesity with Non-Alcoholic Fatty Liver Disease (NAFLD) and Cardiovascular Diseases (CVDs)-The Role of Oxidative Stress.Current issues in molecular biology · 2025Review
- Analysis of the Antioxidant and Antimicrobial Activity, Cytotoxic, and Anti-Migratory Properties of the Essential Oils Obtained from Cultivated MedicinalPlants (Basel, Switzerland) · 2025Article
- Nicotinamide Riboside: A Promising Treatment for Type 1 Cardiorenal Syndrome in Myocardial Infarction-Induced Acute Kidney Injury by Upregulating Nicotinamide Phosphoribosyltransferase-Mediated Nicotinamide Dinucleotide Levels.Journal of the American Heart Association · 2025Article
- The Role of Reductive Stress in the Pathogenesis of Endocrine-Related Metabolic Diseases and Cancer.International journal of molecular sciences · 2025Review
- Sexual Dimorphism of Ethanol-Induced Mitochondrial Dynamics in Purkinje Cells.International journal of molecular sciences · 2024Article
- Drp1 acetylation mediated by CDK5-AMPK-GCN5L1 axis promotes cerebral ischemic injury via facilitating mitochondrial fission.Molecular medicine (Cambridge, Mass.) · 2024Article
- Article
- Brain ethanol metabolism and mitochondria.Current topics in biochemical research · 2022Article
- Review
- Article
- Lipopolysaccharide-Induced Microglial Neuroinflammation: Attenuation by FK866.Neurochemical research · 2021Article
- Article
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 1 country.
Funding
Abstract
It is commonly accepted that mitochondria represent a major source of free radicals following acute brain injury or during the progression of neurodegenerative diseases. The levels of reactive oxygen species (ROS) in cells are determined by two opposing mechanisms-the one that produces free radicals and the cellular antioxidant system that eliminates ROS. Thus, the balance between the rate of ROS production and the efficiency of the cellular detoxification process determines the levels of harmful reactive oxygen species. Consequently, increase in free radical levels can be a result of higher rates of ROS production or due to the inhibition of the enzymes that participate in the antioxidant mechanisms. The enzymes' activity can be modulated by post-translational modifications that are commonly altered under pathologic conditions. In this review we will discuss the mechanisms of mitochondrial free radical production following ischemic insult, mechanisms that protect mitochondria against free radical damage, and the impact of post-ischemic nicotinamide adenine mononucleotide (NAD
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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.