ReviewFrontiers in cardiovascular medicine2018
Calmodulinopathy: Functional Effects of CALM Mutations and Their Relationship With Clinical Phenotypes.
Review in Frontiers in cardiovascular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 35 citations in OpenAlex.
- Calmodulinopathy variants impair CaV1.3 and CaV2.1 regulation.The Journal of general physiology · 2026Article
- Beyond the blueprint: decoding calmodulinopathy-a case report showcasing the utility of multifaceted treatments.European heart journal. Case reports · 2025Article
- The mechanism of LQTS related CaM mutation E141G interfering with CaJournal of physiology and biochemistry · 2025Article
- Antisense Oligonucleotide Therapy for Calmodulinopathy.Circulation · 2024Article
- Calcium Role in Gap Junction Channel Gating: Direct Electrostatic or Calmodulin-Mediated?International journal of molecular sciences · 2024Review
- Epigenetic Modifications of White Blood Cell DNA Caused by Transient Fetal Infection with Bovine Viral Diarrhea Virus.Viruses · 2024Article
- Correspondence between functional scores from deep mutational scans and predicted effects on protein stability.Protein science : a publication of the Protein Society · 2023Article
- Regulation of ErbB Receptors by the CaBiomedicines · 2023Review
- Understanding Calmodulin Variants Affecting Calcium-Dependent Inactivation of L-Type Calcium Channels through Whole-Cell Simulation of the Cardiac Ventricular Myocyte.Biomolecules · 2022Article
- Clinical Characteristics, Genetic Basis and Healthcare Resource Utilisation and Costs in Patients with Catecholaminergic Polymorphic Ventricular Tachycardia: A Retrospective Cohort Study.Reviews in cardiovascular medicine · 2022Article
- Clinical Characteristics, Genetic Findings and Arrhythmic Outcomes of Patients with Catecholaminergic Polymorphic Ventricular Tachycardia from China: A Systematic Review.Life (Basel, Switzerland) · 2022Review
- High value-added application of a renewable bioresource as acaricide: Investigation the mechanism of action of scoparone againstJournal of advanced research · 2022Article
- Clinical Genetics of Inherited Arrhythmogenic Disease in the Pediatric Population.Biomedicines · 2022Review
- How Functional Genomics Can Keep Pace With VUS Identification.Frontiers in cardiovascular medicine · 2022Review
- Calmodulin-Connexin Partnership in Gap Junction Channel Regulation-Calmodulin-Cork Gating Model.International journal of molecular sciences · 2021Review
- The Effect of A2E on the Uptake and Release of Calcium in the Lysosomes and Mitochondria of Human RPE Cells Exposed to Blue Light.Journal of ophthalmology · 2021Article
- The Role of Calmodulin in Tumor Cell Migration, Invasiveness, and Metastasis.International journal of molecular sciences · 2020Review
- Calmodulin mutations and life-threatening cardiac arrhythmias: insights from the International Calmodulinopathy Registry.European heart journal · 2019Article
- Long QT Syndrome Modelling with Cardiomyocytes Derived from Human-induced Pluripotent Stem Cells.Arrhythmia & electrophysiology review · 2019Review
- The Crossroad of Ion Channels and Calmodulin in Disease.International journal of molecular sciences · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In spite of the widespread role of calmodulin (CaM) in cellular signaling, CaM mutations lead specifically to cardiac manifestations, characterized by remarkable electrical instability and a high incidence of sudden death at young age. Penetrance of the mutations is surprisingly high, thus postulating a high degree of functional dominance. According to the clinical patterns, arrhythmogenesis in CaM mutations can be attributed, in the majority of cases, to either prolonged repolarization (as in long-QT syndrome, LQTS phenotype), or to instability of the intracellular Ca
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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.