ReviewBiochimica et biophysica acta2009
Mitochondrial calcium function and dysfunction in the central nervous system.
Review in Biochimica et biophysica acta, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
112 citing papers in PubMed, 1 synthesis or guideline pooled it, 210 citations in OpenAlex.
- Beyond the Mind-Serum Trace Element Levels in Schizophrenic Patients: A Systematic Review.International journal of molecular sciences · 2020Pooled it
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- Mechanistic insights into the synaptic damage-repair and regeneration processes in neurodegenerative Alzheimer's disease: phytochemicals as neuroprotective agents.Frontiers in synaptic neuroscience · 2026Review
- MICU2 controls mitochondrial calcium signaling and migration in neurons during development.Cell reports · 2025Article
- Cognitive dysfunction in chemobrain: Molecular mechanisms and therapeutic implications.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Review
- Beyond the matrix: structural and physiological advancements in mitochondrial calcium signaling.Biochemical Society transactions · 2023Review
- The Transcriptome Profile of Retinal Pigment Epithelium and Müller Cell Lines Protected by Risuteganib Against Hydrogen Peroxide Stress.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2022Article
- Therapeutic Interventions to Mitigate Mitochondrial Dysfunction and Oxidative Stress-Induced Damage in Patients with Bipolar Disorder.International journal of molecular sciences · 2022Review
- Role of Creatine Supplementation in Conditions Involving Mitochondrial Dysfunction: A Narrative Review.Nutrients · 2022Review
- Uncoupling Protein 2 as a Pathogenic Determinant and Therapeutic Target in Cardiovascular and Metabolic Diseases.Current neuropharmacology · 2022Article
- Preventing Axonal Sodium Overload or Mitochondrial Calcium Uptake Protects Axonal Mitochondria from Oxidative Stress-Induced Alterations.Oxidative medicine and cellular longevity · 2022Article
- Localization of Multi-Lamellar Vesicle Nanoparticles to Injured Brain Tissue in a Controlled Cortical Impact Injury Model of Traumatic Brain Injury in Rodents.Neurotrauma reports · 2022Article
- Crosstalk Between the Oxidative Stress and Glia Cells After Stroke: From Mechanism to Therapies.Frontiers in immunology · 2022Review
- Ginsenoside Re Protects against Serotonergic Behaviors Evoked by 2,5-Dimethoxy-4-iodo-amphetamine in Mice via Inhibition of PKCδ-Mediated Mitochondrial Dysfunction.International journal of molecular sciences · 2021Article
- Common Inflammatory Mechanisms in COVID-19 and Parkinson's Diseases: The Role of Microbiome, Pharmabiotics and Postbiotics in Their Prevention.Journal of inflammation research · 2021Review
- Current Evidence on the Protective Effects of Recombinant Human Erythropoietin and Its Molecular Variants against Pathological Hallmarks of Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Guanosine Neuroprotection of Presynaptic Mitochondrial Calcium Homeostasis in a Mouse Study with Amyloid-β Oligomers.Molecular neurobiology · 2020Article
- Kukoamine A Protects against NMDA-Induced Neurotoxicity Accompanied with Down-Regulation of GluN2B-Containing NMDA Receptors and Phosphorylation of PI3K/Akt/GSK-3β Signaling Pathway in Cultured Primary Cortical Neurons.Neurochemical research · 2020Article
- COVID-19 and Parkinson's Disease: Shared Inflammatory Pathways Under Oxidative Stress.Brain sciences · 2020Article
52 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
1 author at 1 institution in 1 country.
Funding
Abstract
The ability of isolated brain mitochondria to accumulate, store and release calcium has been extensively characterized. Extrapolation to the intact neuron led to predictions that the in situ mitochondria would reversibly accumulate Ca(2+) when the concentration of the cation in the vicinity of the mitochondria rose above the 'set-point' at which uptake and efflux were in balance, storing Ca(2+) as a complex with phosphate, and slowly releasing the cation when plasma membrane ion pumps lowered the cytoplasmic free Ca(2+). Excessive accumulation of the cation was predicted to lead to activation of the permeability transition, with catastrophic consequences for the neuron. Each of these predictions has been confirmed with intact neurons, and there is convincing evidence for the permeability transition in cellular Ca(2+) overload associated with glutamate excitotoxicity and stroke, while the neurodegenerative disease in which possible defects in mitochondrial Ca(2+) handling have been most intensively investigated is Huntington's Disease. In this brief review evidence that mitochondrial Ca(2+) transport is relevant to neuronal survival in these conditions will be discussed.
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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.