ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2014
Triadopathies: an emerging class of skeletal muscle diseases.
Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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
44 citing papers in PubMed, 77 citations in OpenAlex.
- The actomyosin cortex controls t-tubule remodeling in skeletal muscle.Science advances · 2026Article
- Beyond Membrane Remodeling: Organelle Crosstalk and Convergent Pathology in Centronuclear Myopathy.Muscles (Basel, Switzerland) · 2026Review
- Review
- Discovery and Treatment of Action Potential-Independent Myotonia in Hyperkalemic Periodic Paralysis.Annals of clinical and translational neurology · 2025Article
- Dominantly inherited muscle disorders: understanding their complexity and exploring therapeutic approaches.Disease models & mechanisms · 2024Review
- Loss-of-function variants inJournal of medical genetics · 2024Article
- Core myopathy in two siblings with a biallelic variant in the CACNA1S gene-A case series study.Clinical case reports · 2024Article
- The Influence of a Genetic Variant inInternational journal of molecular sciences · 2024Article
- Unusual cause of muscle weakness, type II respiratory failure and pulmonary hypertension: a case report of ryanodine receptor type 1(RYR1)-related myopathy.BMC pulmonary medicine · 2024Article
- Nernst-Planck-Gaussian finite element modelling of CaFrontiers in physiology · 2024Article
- Periodic paralysis.Handbook of clinical neurology · 2024Review
- Defective excitation-contraction coupling and mitochondrial respiration precede mitochondrial CaNature communications · 2023Article
- Article
- CaHandbook of experimental pharmacology · 2023Article
- Ryanodine receptor 1 (RYR1) mutations in two patients with tubular aggregate myopathy.The European journal of neuroscience · 2022Article
- Variants in ASPH cause exertional heat illness and are associated with malignant hyperthermia susceptibility.Nature communications · 2022Article
- Centronuclear Myopathy Caused by Defective Membrane Remodelling of Dynamin 2 and BIN1 Variants.International journal of molecular sciences · 2022Review
- Numb is required for optimal contraction of skeletal muscle.Journal of cachexia, sarcopenia and muscle · 2022Article
- Finite element analysis predicts CaScientific reports · 2021Article
- Striated Preferentially Expressed Protein Kinase (SPEG) in Muscle Development, Function, and Disease.International journal of molecular sciences · 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
3 authors at 3 institutions in 2 countries.
Funding
Abstract
The triad is a skeletal muscle substructure responsible for the regulation of excitation-contraction coupling. It is formed by the close apposition of the T-tubule and the terminal sarcoplasmic reticulum. A rapidly growing list of skeletal myopathies, here referred to as triadopathies, are caused by gene mutations in components of the triad. These disorders, at their root, are caused by defects in excitation contraction coupling and intracellular calcium homeostasis. Secondary abnormalities in triad structure and/or function are also reported in several muscle diseases, most notably certain muscular dystrophies. This review highlights the current understanding of both primary and secondary triadopathies, and identifies important concepts yet to be fully addressed in the field. The emphasis of the review is both on the pathogenesis of triadopathies and their potential treatment.
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.