ArticlePharmaceuticals (Basel, Switzerland)2013
Voltage-gated calcium channel antagonists and traumatic brain injury.
Article in Pharmaceuticals (Basel, Switzerland), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- N-Type Ca Channel in Epileptic Syndromes and Epilepsy: A Systematic Review of Its Genetic Variants.International journal of molecular sciences · 2023Pooled it
- Calcium Signaling in Astrocytes and Its Role in the Central Nervous System Injury.Molecular neurobiology · 2025Review
- Blocking axon-glial mechanotransduction to prevent concussive brain injury.Acta neuropathologica communications · 2025Article
- Genetic Differences Modify Anesthetic Preconditioning of Traumatic Brain Injury in Drosophila.Journal of neurotrauma · 2025Article
- Mechanistic investigation of methadone, tolfenamic acid, and cilnidipine in traumatic brain injury: a novel multi-target perspective outcome of network pharmacology.Inflammopharmacology · 2025Article
- Neurological Manifestations Following Traumatic Brain Injury: Role of Behavioral, Neuroinflammation, Excitotoxicity, Nrf-2 and Nitric Oxide.CNS & neurological disorders drug targets · 2025Review
- Mesenchymal stem cells and their extracellular vesicle therapy for neurological disorders: traumatic brain injury and beyond.Frontiers in neurology · 2025Review
- Calcium and Non-Penetrating Traumatic Brain Injury: A Proposal for the Implementation of an Early Therapeutic Treatment for Initial Head Insults.Biomolecules · 2024Review
- Anatomical Features and Material Properties of Human Surrogate Head Models Affect Spatial and Temporal Brain Motion under Blunt Impact.Bioengineering (Basel, Switzerland) · 2024Article
- Dynamic Changes in Ion Channels during Myocardial Infarction and Therapeutic Challenges.International journal of molecular sciences · 2024Review
- Sildenafil amplifies calcium influx and insulin secretion in pancreatic β cells.Physiological reports · 2024Article
- Blood-testis barrier: a review on regulators in maintaining cell junction integrity between Sertoli cells.Cell and tissue research · 2024Review
- Electrolyte Imbalance and Neurologic Injury.CNS & neurological disorders drug targets · 2024Review
- Regulation of N-type calcium channels by nociceptin receptors and its possible role in neurological disorders.Molecular brain · 2022Review
- A mechanistic model of calcium homeostasis leading to occurrence and propagation of secondary brain injury.Journal of neurophysiology · 2022Article
- Article
- Trimethyltin Increases Intracellular CaMolecular neurobiology · 2021Article
- Nimodipine Promotes Functional Recovery After Spinal Cord Injury in Rats.Frontiers in pharmacology · 2021Article
- Transcriptional Pathology Evolves over Time in Rat Hippocampus after Lateral Fluid Percussion Traumatic Brain Injury.Neurotrauma reports · 2021Article
- Sigma-1 Receptor: A Potential Therapeutic Target for Traumatic Brain Injury.Frontiers in cellular neuroscience · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is a leading cause of death and disability in the United States. Despite more than 30 years of research, no pharmacological agents have been identified that improve neurological function following TBI. However, several lines of research described in this review provide support for further development of voltage gated calcium channel (VGCC) antagonists as potential therapeutic agents. Following TBI, neurons and astrocytes experience a rapid and sometimes enduring increase in intracellular calcium ([Ca2+]i). These fluxes in [Ca2+]i drive not only apoptotic and necrotic cell death, but also can lead to long-term cell dysfunction in surviving cells. In a limited number of in vitro experiments, both L-type and N-type VGCC antagonists successfully reduced calcium loads as well as neuronal and astrocytic cell death following mechanical injury. In rodent models of TBI, administration of VGCC antagonists reduced cell death and improved cognitive function. It is clear that there is a critical need to find effective therapeutics and rational drug delivery strategies for the management and treatment of TBI, and we believe that further investigation of VGCC antagonists should be pursued before ruling out the possibility of successful translation to the clinic.
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.