ReviewThe Journal of physiology2020
Molecular and tissue mechanisms of catecholaminergic polymorphic ventricular tachycardia.
Review in The Journal of physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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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.
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.
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Who cites it
68 citing papers in PubMed, 118 citations in OpenAlex.
- A Mechanistic Clinical Trial Using (Circulation. Arrhythmia and electrophysiology · 2022Trial
- Optical mapping: pioneering the frontier of preclinical antiarrhythmic drug evaluation.iScience · 2026Review
- Structural and Functional Regulation of RyR2 in Cardiac Calcium Handling and Arrhythmogenesis.Biomedicines · 2026Review
- Ca2+ signalling in cardiac muscle: the importance of balances.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026Review
- Ryanodine receptor 2 mutations in catecholaminergic polymorphic ventricular tachycardia: From molecular mechanisms to precision medicine.World journal of cardiology · 2026Review
- Neural Regulation of Cardiac Arrhythmias: From the Brain-Heart Axis to Emerging Precision Therapies.Research (Washington, D.C.) · 2026Review
- Catecholaminergic polymorphic ventricular tachycardia: A narrative review of recent advances in genetics, mechanisms, diagnosis, and treatment.Asian heart journal · 2025Review
- Compromised repolarization reserve in a murine model of catecholaminergic polymorphic ventricular tachycardia caused by RyR2-R420Q mutation.Journal of molecular and cellular cardiology · 2025Article
- Pharmacological Enhancement of Small Conductance CaCirculation research · 2025Article
- Distinct intracellular spatiotemporal expression of Calmodulin genes underlies functional diversity of Calmodulin-dependent signalling in cardiac myocytes.Cardiovascular research · 2025Article
- Cardiac Channelopathies: Clinical Diagnosis and Promising Therapeutics.Journal of the American Heart Association · 2025Review
- Extracorporeal membrane oxygenation for catecholaminergic polymorphic ventricular tachycardia: a case report and literature review.BMC pediatrics · 2025Review
- Heart on Fire: UnmaskingMethodist DeBakey cardiovascular journal · 2025Article
- Dual calcium-voltage optical mapping of regional voltage and calcium signals in intact murineJournal of molecular and cellular cardiology plus · 2024Article
- Potential Therapeutic Targets for Hypotension in Duchenne Muscular Dystrophy.Medical hypotheses · 2024Article
- Catecholaminergic Polymorphic Ventricular Tachycardia: Clinical Characteristics, Diagnostic Evaluation and Therapeutic Strategies.Journal of clinical medicine · 2024Review
- A dual-targeted drug inhibits cardiac ryanodine receptor CaLife science alliance · 2024Article
- CardiOmics signatures reveal therapeutically actionable targets and drugs for cardiovascular diseases.Heliyon · 2024Article
- Inherited Arrhythmias in the Pediatric Population: An Updated Overview.Medicina (Kaunas, Lithuania) · 2024Review
- Inhibitory effect of aloperine on transient outward potassium currents in rat cardiac myocytes.Frontiers in pharmacology · 2024Article
8 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a stress-induced cardiac channelopathy that has a high mortality in untreated patients. Our understanding has grown tremendously since CPVT was first described as a clinical syndrome in 1995. It is now established that the deadly arrhythmias are caused by unregulated 'pathological' calcium release from the sarcoplasmic reticulum (SR), the major calcium storage organelle in striated muscle. Important questions remain regarding the molecular mechanisms that are responsible for the pathological calcium release, regarding the tissue origin of the arrhythmic beats that initiate ventricular tachycardia, and regarding optimal therapeutic approaches. At present, mutations in six genes involved in SR calcium release have been identified as the genetic cause of CPVT: RYR2 (encoding ryanodine receptor calcium release channel), CASQ2 (encoding cardiac calsequestrin), TRDN (encoding triadin), CALM1, CALM2 and CALM3 (encoding identical calmodulin protein). Here, we review each CPVT subtype and how CPVT mutations alter protein function, RyR2 calcium release channel regulation, and cellular calcium handling. We then discuss research and hypotheses surrounding the tissue mechanisms underlying CPVT, such as the pathophysiological role of sinus node dysfunction in CPVT, and whether the arrhythmogenic beats originate from the conduction system or the ventricular working myocardium. Finally, we review the treatments that are available for patients with CPVT, their efficacy, and how therapy could be improved in the future.
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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.