ReviewCurrent molecular pharmacology2015
Calcium Channel Mutations in Cardiac Arrhythmia Syndromes.
Review in Current molecular pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 62 citations in OpenAlex.
- Differential expression of genes participating in cardiomyocyte electrophysiological remodeling via membrane ionic mechanisms and CaMolecular and cellular biochemistry · 2020Trial
- C-Terminus of CaCells · 2026Article
- BMAL1 mediates sex-specific circadian regulation of cardiac ion channels and temporal arrhythmia vulnerability.Heart rhythm · 2026Article
- Expanding clinical phenotype in CACNA1C related disorders: familial mesial temporal lobe epilepsy.Acta epileptologica · 2025Article
- Autoimmune antibodies in arrhythmia: a narrative review of potential therapeutic targets to prevent overtreatment.Cardiovascular diagnosis and therapy · 2025Review
- Multi-Omics Approach Reveals Genes and Pathways Affected in Miller-Dieker Syndrome.Molecular neurobiology · 2025Article
- Updates on Intrinsic Medicinal Chemistry of 1,4-dihydropyridines, Perspectives on Synthesis and Pharmacokinetics of Novel 1,4-dihydropyrimidines as Calcium Channel Blockers: Clinical Pharmacology.Current topics in medicinal chemistry · 2025Review
- Toxicity profiles of immune checkpoint inhibitors in nervous system cancer: a comprehensive disproportionality analysis using FDA adverse event reporting system.Clinical and experimental medicine · 2024Article
- Electrophysiological Mechanism of Catestatin Antiarrhythmia: Enhancement ofJournal of the American Heart Association · 2024Article
- The Dysfunction of CaInternational journal of molecular sciences · 2023Review
- Review
- Synthesis of Dihydropyrimidines: Isosteres of Nifedipine and Evaluation of Their Calcium Channel Blocking Efficiency.Molecules (Basel, Switzerland) · 2023Review
- Analysis ofGenes · 2022Article
- Therapeutic Potential of Targeting Regulated Intramembrane Proteolysis Mechanisms of Voltage-Gated Ion Channel Subunits and Cell Adhesion Molecules.Pharmacological reviews · 2022Review
- A next generation sequencing gene panel for use in the diagnosis of anorexia nervosa.Eating and weight disorders : EWD · 2022Article
- Review
- Taiji-reprogram: a framework to uncover cell-type specific regulators and predict cellular reprogramming cocktails.NAR genomics and bioinformatics · 2021Article
- iPSC-derived cardiomyocytes from patients with myotonic dystrophy type 1 have abnormal ion channel functions and slower conduction velocities.Scientific reports · 2021Article
- Commentary: Peptide-Based Targeting of the L-Type Calcium Channel Corrects the Loss-of-Function Phenotype of Two Novel Mutations of theFrontiers in physiology · 2021Article
- Cav1.2 channelopathies causing autism: new hallmarks on Timothy syndrome.Pflugers Archiv : European journal of physiology · 2020Review
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 1 institution in 1 country.
Funding
Abstract
Voltage gated calcium channels are essential for cardiac physiology by serving as sarcolemma- restricted gatekeepers for calcium in cardiac myocytes. Activation of the L-type voltagegated calcium channel provides the calcium entry required for excitation-contraction coupling and contributes to the plateau phase of the cardiac action potential. Given these critical physiological roles, subtle disturbances in L-type channel function can lead to fatal cardiac arrhythmias. Indeed, numerous human arrhythmia syndromes have been linked to mutations in the L-type channel leading to gain-of-function or loss-of-function mutations. In this review, we discuss the current state of knowledge regarding these mutations present in Timothy Syndrome, Long and Short QT Syndromes, Brugada Syndrome and Early Repolarization Syndrome. We discuss the pathological consequences of the mutations, the biophysical effects of the mutations on the channel as well as possible therapeutic considerations and challenges for future studies.
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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.