ReviewTranslational stroke research2013
Mitochondrial dysfunction and NAD(+) metabolism alterations in the pathophysiology of acute brain injury.
Review in Translational stroke research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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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
31 citing papers in PubMed, 49 citations in OpenAlex.
- Mitochondrial alterations in pellagra-associated central chromatolysis: Comparison with ballooned achromatic neurons of other etiologies.Journal of neuropathology and experimental neurology · 2026Article
- Cognitive impairment following maternal separation in rats mediated by the NADTranslational psychiatry · 2025Article
- Administration of AICAR, an AMPK Activator, Prevents and Reverses Diabetic Polyneuropathy (DPN) by Regulating Mitophagy.International journal of molecular sciences · 2024Article
- Tetramethylpyrazine protects mitochondrial function by up-regulation of TFAM and inhibition of neuronal apoptosis in a rat model of surgical brain injury.Iranian journal of basic medical sciences · 2024Article
- Identification of late-life depression and mild cognitive impairment via serum surface-enhanced Raman spectroscopy and multivariate statistical analysis.Biomedical optics express · 2023Article
- Review
- Exploration of the Molecular Mechanisms Underlying the Anti-Photoaging Effect ofFrontiers in cellular and infection microbiology · 2022Article
- Endoplasmic Reticulum Interaction Supports Energy Production and Redox Homeostasis in Mitochondria Released from Astrocytes.Translational stroke research · 2021Article
- Different Roles of Mitochondria in Cell Death and Inflammation: Focusing on Mitochondrial Quality Control in Ischemic Stroke and Reperfusion.Biomedicines · 2021Review
- Role of NADBrain sciences · 2020Review
- Ischemic Neuroprotectant PKCε Restores Mitochondrial Glutamate Oxaloacetate Transaminase in the Neuronal NADH Shuttle after Ischemic Injury.Translational stroke research · 2020Article
- Nicotinamide Mononucleotide Administration Prevents Experimental Diabetes-Induced Cognitive Impairment and Loss of Hippocampal Neurons.International journal of molecular sciences · 2020Article
- Mitochondrial Functions, Energy Metabolism and Protein Glycosylation are Interconnected Processes Mediating Resistance to Bortezomib in Multiple Myeloma Cells.Biomolecules · 2020Article
- Mitochondrial Protection by PARP Inhibition.International journal of molecular sciences · 2020Review
- NADExperimental neurology · 2020Review
- Multi-targeted Effect of Nicotinamide Mononucleotide on Brain Bioenergetic Metabolism.Neurochemical research · 2019Review
- Interplay between NADBiochimica et biophysica acta. Molecular basis of disease · 2019Review
- Nicotinamide mononucleotide alters mitochondrial dynamics by SIRT3-dependent mechanism in male mice.Journal of neuroscience research · 2019Article
- Role of mitochondrial calcium uniporter-mediated CaJournal of cellular and molecular medicine · 2019Article
- Significance of Mitochondrial Protein Post-translational Modifications in Pathophysiology of Brain Injury.Translational stroke research · 2018Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mitochondrial dysfunction is commonly believed to be one of the major players in mechanisms of brain injury. For several decades, pathologic mitochondrial calcium overload and associated opening of the mitochondrial permeability transition (MPT) pore were considered a detrimental factor causing mitochondrial damage and bioenergetics failure. Mitochondrial and cellular bioenergetic metabolism depends on the enzymatic reactions that require NAD(+) or its reduced form NADH as cofactors. Recently, it was shown that NAD(+) also has an important function as a substrate for several NAD(+) glycohydrolases whose overactivation can contribute to cell death mechanisms. Furthermore, downstream metabolites of NAD(+) catabolism can also adversely affect cell viability. In contrast to the negative effects of NAD(+)-catabolizing enzymes, enzymes that constitute the NAD(+) biosynthesis pathway possess neuroprotective properties. In the first part of this review, we discuss the role of MPT in acute brain injury and its role in mitochondrial NAD(+) metabolism. Next, we focus on individual NAD(+) glycohydrolases, both cytosolic and mitochondrial, and their role in NAD(+) catabolism and brain damage. Finally, we discuss the potential effects of downstream products of NAD(+) degradation and associated enzymes as well as the role of NAD(+) resynthesis enzymes as potential therapeutic targets.
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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.