ReviewCells2021
Ion Channel Gene Mutations Causing Skeletal Muscle Disorders: Pathomechanisms and Opportunities for Therapy.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- The Role of Electrolytes in Muscle Pain Syndromes: A Systematic Review and Meta-Analysis With Implications for Temporomandibular Disorder.International dental journal · 2026Pooled it
- Alternative splicing in voltage-gated sodium channels: mechanisms, regulatory networks and therapeutic implications.Annals of medicine · 2026Review
- Review
- Steroid-induced Hypokalemic Periodic Paralysis.Annals of African medicine · 2026Article
- Rhabdomyolysis: a narrative review.Arquivos de neuro-psiquiatria · 2026Review
- Efficacy of Retigabine in Treating Weakness in a Mouse Model of Hypokalemic Periodic Paralysis.Muscle & nerve · 2026Article
- Thyrotoxic Hypokalemic Periodic Paralysis: Pathophysiological Mechanisms.Endocrinology and metabolism (Seoul, Korea) · 2025Review
- Identification of Novel Genomic Variants in COVID-19 Patients Using Whole-Exome Sequencing: Exploring the Plausible Targets of Functional Genomics.Biochemical genetics · 2025Article
- Donepezil treatment, alone or combined with exercise, enhances skeletal muscle function in healthy and advanced aging disease mouse models.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Article
- Nonsteroidal Anti-Inflammatory Drugs as Modulators of Cation Channels: Fenamates Repurposing in Channelopathies.ChemMedChem · 2025Review
- Discovery and Treatment of Action Potential-Independent Myotonia in Hyperkalemic Periodic Paralysis.Annals of clinical and translational neurology · 2025Article
- Article
- Pleiotropic Effects of the NSAID Fenamates on Chloride Channels: Opportunity for Ion Channelopathies?Pharmacology research & perspectives · 2025Review
- Chloride channels and mast cell function: pioneering new frontiers in IBD therapy.Molecular and cellular biochemistry · 2025Review
- Mechanisms underlying the distinct K+ dependencies of periodic paralysis.The Journal of general physiology · 2025Article
- Pharmacological therapy of non-dystrophic myotonias.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2025Review
- Unlocking the Secrets of Andersen-Tawil Syndrome: The Role of Next-Generation Sequencing in a Family With Long QT Syndrome.Cardiology research and practice · 2025Article
- BK channels promote action potential repolarization in skeletal muscle but contribute little to myotonia.Pflugers Archiv : European journal of physiology · 2024Article
- Reduced KThe Journal of physiology · 2024Article
- Preclinical study of the antimyotonic efficacy of safinamide in the myotonic mouse model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
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
Abstract
Skeletal muscle ion channelopathies (SMICs) are a large heterogeneous group of rare genetic disorders caused by mutations in genes encoding ion channel subunits in the skeletal muscle mainly characterized by myotonia or periodic paralysis, potentially resulting in long-term disabilities. However, with the development of new molecular technologies, new genes and new phenotypes, including progressive myopathies, have been recently discovered, markedly increasing the complexity in the field. In this regard, new advances in SMICs show a less conventional role of ion channels in muscle cell division, proliferation, differentiation, and survival. Hence, SMICs represent an expanding and exciting field. Here, we review current knowledge of SMICs, with a description of their clinical phenotypes, cellular and molecular pathomechanisms, and available treatments.
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.