ArticleFrontiers in neuroenergetics2013
Concentration dependent effect of calcium on brain mitochondrial bioenergetics and oxidative stress parameters.
Article in Frontiers in neuroenergetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 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
61 citing papers in PubMed, 120 citations in OpenAlex.
- Involvement of mitochondrial pathway in environmental metal pollutant lead-induced apoptosis of chicken liver: perspectives from oxidative stress and energy metabolism.Environmental science and pollution research international · 2017Trial
- Changes in metabolites after treatment with memantine in fibromyalgia. A double-blind randomized controlled trial with magnetic resonance spectroscopy with a 6-month follow-up.CNS neuroscience & therapeutics · 2014Trial
- Exploring Replicative Senescence and Oxidative Stress-Induced Remodelling of Mitochondrial-Associated Membranes in Human Skin Fibroblasts.Biomolecules · 2026Article
- Elevating levels of neuronal MCU in the hippocampus enhances mitochondrial calcium uptake and respiratory efficiency proportional to demand.bioRxiv : the preprint server for biology · 2026Article
- A perspective on the future of heart failure research.Journal of molecular and cellular cardiology plus · 2026Article
- A novel strategy to target metabolic dependencies in acute myeloid leukemia.Cell death & disease · 2025Article
- A Pharmacological Perspective on Targeting the Voltage-Gated Calcium Channel Subunit αNeurochemical research · 2025Review
- Neurological Manifestations Following Traumatic Brain Injury: Role of Behavioral, Neuroinflammation, Excitotoxicity, Nrf-2 and Nitric Oxide.CNS & neurological disorders drug targets · 2025Review
- Mitigating neuroinflammation in cognitive areas: exploring the impact of HMG-CoA reductase inhibitor.The Biochemical journal · 2024Article
- Enhanced mitochondrial buffering prevents CaThe Journal of physiology · 2024Article
- Targeting Acute Myeloid Leukemia Stem Cells through Perturbation of Mitochondrial Calcium.Cancer discovery · 2024Article
- The Uncoupling Effect of 17β-Estradiol Underlies the Resilience of Female-Derived Mitochondria to Damage after Experimental TBI.Life (Basel, Switzerland) · 2024Article
- An efficient and high-throughput method for the evaluation of mitochondrial dysfunction in frozen brain samples after traumatic brain injury.Frontiers in molecular biosciences · 2024Article
- Crosstalk between adenine nucleotide transporter and mitochondrial swelling: experimental and computational approaches.Cell biology and toxicology · 2023Article
- Antagonistic Interactions in Mitochondria ROS Signaling Responses to Manganese.Antioxidants (Basel, Switzerland) · 2023Article
- CDDO-Me Abrogates Aberrant Mitochondrial Elongation in Clasmatodendritic Degeneration by Regulating NF-κB-PDI-Mediated S-Nitrosylation of DRP1.International journal of molecular sciences · 2023Article
- Characterizing Sex Differences in Mitochondrial Dysfunction After Severe Traumatic Brain Injury in Mice.Neurotrauma reports · 2023Article
- Overexpression ofCells · 2022Article
- CDDO-Me Attenuates Clasmatodendrosis in CA1 Astrocyte by Inhibiting HSP25-AKT Mediated DRP1-S637 Phosphorylation in Chronic Epilepsy Rats.International journal of molecular sciences · 2022Article
- Mesenchymal stromal cell-derived extracellular vesicles afford neuroprotection by modulating PI3K/AKT pathway and calcium oscillations.International journal of biological sciences · 2022Article
1 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
Mitochondrial dysfunction following traumatic brain and spinal cord injury (TBI and SCI) plays a pivotal role in the development of secondary pathophysiology and subsequent neuronal cell death. Previously, we demonstrated a loss of mitochondrial bioenergetics in the first 24 h following TBI and SCI initiates a rapid and extensive necrotic event at the primary site of injury. Within the mitochondrial derived mechanisms, the cross talk and imbalance amongst the processes of excitotoxicity, Ca(2+) cycling/overload, ATP synthesis, free radical production and oxidative damage ultimately lead to mitochondrial damage followed by neuronal cell death. Mitochondria are one of the important organelles that regulate intracellular calcium (Ca(2+)) homeostasis and are equipped with a tightly regulated Ca(2+) transport system. However, owing to the lack of consensus and the link between downstream effects of calcium in published literature, we undertook a systematic in vitro study for measuring concentration dependent effects of calcium (100-1000 nmols/mg mitochondrial protein) on mitochondrial respiration, enzyme activities, reactive oxygen/nitrogen species (ROS/RNS) generation, membrane potential (ΔΨ) and oxidative damage markers in isolated brain mitochondria. We observed a dose- and time-dependent inhibition of mitochondrial respiration by calcium without influencing mitochondrial pyruvate dehydrogenase complex (PDHC) and NADH dehydrogenase (Complex I) enzyme activities. We observed dose-dependent decreased production of hydrogen peroxide and total ROS/RNS species generation by calcium and no significant changes in protein and lipid oxidative damage markers. These results may shed new light on the prevailing dogma of the direct effects of calcium on mitochondrial bioenergetics, free radical production and oxidative stress parameters that are primary regulatory mitochondrial mechanisms following neuronal injury.
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.