ArticleCurrent neuropharmacology2013
The changing landscape of voltage-gated calcium channels in neurovascular disorders and in neurodegenerative diseases.
Article in Current neuropharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Cell adhesion and intracellular calcium signaling in neurons.Cell communication and signaling : CCS · 2013Pooled it
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- Research developments in the neurovascular unit and the blood‑brain barrier (Review).Biomedical reports · 2025Review
- STIM Proteins: The Gas and Brake of Calcium Entry in Neurons.Neuroscience bulletin · 2025Review
- The senescent synapse: A look at autophagy, calcium handling, and mitochondrial bioenergetics at the synapse in ageing and Parkinson's disease.Current research in physiology · 2025Review
- Mechanism of LCN2 in cerebral ischemia-reperfusion injury.Frontiers in neuroscience · 2025Review
- Causal association between gut microbiomes and different types of aneurysms: a Mendelian randomization study.Frontiers in microbiology · 2024Article
- Extracellular high molecular weight α-synuclein oligomers induce cell death by disrupting the plasma membrane.NPJ Parkinson's disease · 2023Article
- A mechanistic model of calcium homeostasis leading to occurrence and propagation of secondary brain injury.Journal of neurophysiology · 2022Article
- Melatonin attenuates cerebral hypoperfusion-induced hippocampal damage and memory deficits in rats by suppressing TRPM7 channels.Saudi journal of biological sciences · 2022Article
- CaInternational journal of molecular sciences · 2022Review
- COVID-19, Cation Dysmetabolism, Sialic Acid, CD147, ACE2, Viroporins, Hepcidin and Ferroptosis: A Possible Unifying Hypothesis.F1000Research · 2022Review
- Review
- Retinal Vessel Responses to Flicker Stimulation Are Impaired in CaFrontiers in neurology · 2021Article
- Alzheimer's disease risk geneeLife · 2020Article
- Amyloid, APP, and Electrical Activity of the Brain.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2020Review
- Voltage-Gated Calcium Channels and α-Synuclein: Implications in Parkinson's Disease.Frontiers in molecular neuroscience · 2019Review
- Integrated identification of key genes and pathways in Alzheimer's disease via comprehensive bioinformatical analyses.Hereditas · 2019Article
- Synthesis and Biological Evaluations of NO-Donating Oxa- and Aza-Pentacycloundecane Derivatives as Potential Neuroprotective Candidates.Molecules (Basel, Switzerland) · 2018Article
- Pathophysiologic relationship between Alzheimer's disease, cerebrovascular disease, and cardiovascular risk: A review and synthesis.Alzheimer's & dementia (Amsterdam, Netherlands) · 2017Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is a common belief that voltage-gated calcium channels (VGCC) cannot carry toxic amounts of Ca(2+) in neurons. Also, some of them as L-type channels are essential for Ca(2+)-dependent regulation of prosurvival gene-programs. However, a wealth of data show a beneficial effect of drugs acting on VGCCs in several neurodegenerative and neurovascular diseases. In the present review, we explore several mechanisms by which the "harmless" VGCCs may become "toxic" for neurons. These mechanisms could explain how, though usually required for neuronal survival, VGCCs may take part in neurodegeneration. We will present evidence showing that VGCCs can carry toxic Ca(2+) when: a) their density or activity increases because of aging, chronic hypoxia or exposure to β-amyloid peptides or b) Ca(2+)-dependent action potentials carry high Ca(2+) loads in pacemaker neurons. Besides, we will examine conditions in which VGCCs promote neuronal cell death without carrying excess Ca(2+). This can happen, for instance, when they carry metal ions into the neuronal cytoplasm or when a pathological decrease in their activity weakens Ca(2+)-dependent prosurvival gene programs. Finally, we will explore the role of VGCCs in the control of nonneuronal cells that take part to neurodegeneration like those of the neurovascular unit or of microglia.
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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.