ReviewFrontiers in pharmacology2020
Epilepsy-Related Voltage-Gated Sodium Channelopathies: A Review.
Review in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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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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Who cites it
79 citing papers in PubMed, 134 citations in OpenAlex.
- Functional and pharmacological characterization of theEpilepsy & behavior reports · 2026Article
- Advancing the Paradigm of Temporal Lobe Epilepsy as a Network Disease: The Promise of Biomarkers and Targeted Disease Modification.International journal of molecular sciences · 2026Review
- Lvguidingan inhibits Nav1.2 and epilepsy-associated SCN2A gain-of-function variants.Acta pharmacologica Sinica · 2026Article
- Structure and function of voltage-gated sodium channel Nav1.6: Involvement in the pathological process of neural injury.Neural regeneration research · 2026Article
- Integrative Drug-Target Causal Analysis, Single-Cell Sequencing and In-Vivo Validation for Dissecting Molecular Mechanisms Underlying Focal Epilepsy.CNS neuroscience & therapeutics · 2026Article
- Identification of a Novel Homozygous SCN1B Splice-Site Variant in a Consanguineous Families With Early-Onset Epilepsy: A Case Series and Review of Literature.Molecular genetics & genomic medicine · 2026Review
- Modern Analytical Techniques in Epilepsy Research.International journal of molecular sciences · 2026Review
- Cardiovascular morbidity following epilepsy: A nationwide retrospective cohort study in South Korea.Epilepsia open · 2026Article
- Functional Characterization of a De NovoNeurology. Genetics · 2026Article
- Exceptionally selective voltage-sensor trapping of NaScientific reports · 2026Article
- Ancestral intronic splicing regulatory elements in the SCNbioRxiv : the preprint server for biology · 2026Article
- Shared Disease Mechanisms in Neurodevelopmental Disorders: A Cellular and Molecular Biology Perspective.Brain sciences · 2025Review
- Neurologist's Black Swan: Molecular Basis of Prenatal Seizures.International journal of molecular sciences · 2025Review
- Article
- The cost of unmodeled biological complexity in artificial neural networks.Patterns (New York, N.Y.) · 2025Review
- Voltage-Gated Sodium Channel Dysfunction in Epilepsy: Zebrafish Models for Therapeutics.Biomedicines · 2025Review
- Differential roles of NaeLife · 2025Article
- Transcriptomic analyses of human brains with Alzheimer's disease identified dysregulated epilepsy-causing genes.Epilepsy & behavior : E&B · 2025Article
- Pathogenic variants in the polycystin pore helix cause distinct forms of channel dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- H- and m-channel overexpression promotes seizure-like events by impairing the ability of inhibitory neurons to process correlated inputs.PLoS computational biology · 2025Article
19 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
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epilepsy is a disease characterized by abnormal brain activity and a predisposition to generate epileptic seizures, leading to neurobiological, cognitive, psychological, social, and economic impacts for the patient. There are several known causes for epilepsy; one of them is the malfunction of ion channels, resulting from mutations. Voltage-gated sodium channels (NaV) play an essential role in the generation and propagation of action potential, and malfunction caused by mutations can induce irregular neuronal activity. That said, several genetic variations in NaV channels have been described and associated with epilepsy. These mutations can affect channel kinetics, modifying channel activation, inactivation, recovery from inactivation, and/or the current window. Among the NaV subtypes related to epilepsy, NaV1.1 is doubtless the most relevant, with more than 1500 mutations described. Truncation and missense mutations are the most observed alterations. In addition, several studies have already related mutated NaV channels with the electrophysiological functioning of the channel, aiming to correlate with the epilepsy phenotype. The present review provides an overview of studies on epilepsy-associated mutated human NaV1.1, NaV1.2, NaV1.3, NaV1.6, and NaV1.7.
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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.