ReviewComprehensive Physiology2015
Channelopathies of skeletal muscle excitability.
Review in Comprehensive Physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers, 1 of them a synthesis that pooled it.
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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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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
138 citing papers in PubMed, 1 synthesis or guideline pooled it, 213 citations in OpenAlex.
- Targeted Therapies for Skeletal Muscle Ion Channelopathies: Systematic Review and Steps Towards Precision Medicine.Journal of neuromuscular diseases · 2021Pooled it
- Mexiletine in spinal and bulbar muscular atrophy: a randomized controlled trial.Annals of clinical and translational neurology · 2022Trial
- Open-Label, Dose-Escalation, Phase 1 Study of Safety and Single and Multiple-Dose Pharmacokinetics of Dichlorphenamide in Healthy Volunteers.Clinical pharmacology in drug development · 2019Trial
- A bifunctional actuator to correct loss-of-function deficits in cardiac voltage-gated sodium channels.Science advances · 2026Article
- Study of enhancing analgesic potential of μ-conotoxins from the computational and pharmacological insights.Molecular diversity · 2026Article
- Treatment updates in myotonic disorders.Journal of neurology · 2026Review
- The hallmarks of skeletal muscle health.Nature metabolism · 2026Review
- Peptide Coacervates as Dynamic and Interactive Depots for Tetrodotoxin in Long-Acting Local Anesthesia.Advanced healthcare materials · 2026Article
- Efficacy of sodium channel blockers in treating myotonia is independent of action potential sodium current block.The Journal of physiology · 2026Article
- Article
- Cholesterol-depleting dextrin depolarizes sarcolemma: the contribution of sodium / calcium channels and membrane integrity.Pflugers Archiv : European journal of physiology · 2026Article
- Article
- Efficacy of Retigabine in Treating Weakness in a Mouse Model of Hypokalemic Periodic Paralysis.Muscle & nerve · 2026Article
- Efficacy of a KMuscle & nerve · 2026Article
- Review
- Uncovering the genetic architecture of ME/CFS: a precision approach reveals impact of rare monogenic variation.Journal of translational medicine · 2025Article
- Myotonic dystrophy type 1: clinical diversity, molecular insights and therapeutic perspectives.Nature reviews. Neurology · 2025Review
- Discovery and Treatment of Action Potential-Independent Myotonia in Hyperkalemic Periodic Paralysis.Annals of clinical and translational neurology · 2025Article
- Biophysical and structural insights into the SCN4A E452K variant linked to myotonia and paramyotonia congenita.Scientific reports · 2025Article
- Elimination of myotonia improves myopathy in a muscleblind knockout model of myotonic dystrophy.bioRxiv : the preprint server for biology · 2025Article
78 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
Familial disorders of skeletal muscle excitability were initially described early in the last century and are now known to be caused by mutations of voltage-gated ion channels. The clinical manifestations are often striking, with an inability to relax after voluntary contraction (myotonia) or transient attacks of severe weakness (periodic paralysis). An essential feature of these disorders is fluctuation of symptoms that are strongly impacted by environmental triggers such as exercise, temperature, or serum K(+) levels. These phenomena have intrigued physiologists for decades, and in the past 25 years the molecular lesions underlying these disorders have been identified and mechanistic studies are providing insights for therapeutic strategies of disease modification. These familial disorders of muscle fiber excitability are "channelopathies" caused by mutations of a chloride channel (ClC-1), sodium channel (NaV1.4), calcium channel (CaV1.1), and several potassium channels (Kir2.1, Kir2.6, and Kir3.4). This review provides a synthesis of the mechanistic connections between functional defects of mutant ion channels, their impact on muscle excitability, how these changes cause clinical phenotypes, and approaches toward therapeutics.
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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.