ReviewThe Journal of physiology2015
Deranged sodium to sudden death.
Review in The Journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 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
32 citing papers in PubMed, 56 citations in OpenAlex.
- A bifunctional actuator to correct loss-of-function deficits in cardiac voltage-gated sodium channels.Science advances · 2026Article
- Pharmacological and Non-Pharmacological Interventions in Diabetes Mellitus: Effects on Epicardial Adipose Tissue.International journal of molecular sciences · 2025Review
- SGLT2 Inhibitors and How They Work Beyond the Glucosuric Effect. State of the Art.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2024Review
- CARDS, a Novel Prognostic Index for Risk Stratification and In-Hospital Monitoring.Journal of clinical medicine · 2024Article
- A new approach to characterize cardiac sodium storage by combining fluorescence photometry and magnetic resonance imaging in small animal research.Scientific reports · 2024Article
- Health position paper and redox perspectives on reactive oxygen species as signals and targets of cardioprotection.Redox biology · 2023Review
- New insights on cardiac Na channel block by an atypical anti-arrhythmic drug.Nature cardiovascular research · 2023Article
- Fibroblast growth factor homologous factors serve as a molecular rheostat in tuning arrhythmogenic cardiac late sodium current.Nature cardiovascular research · 2022Article
- Frequency-Dependent Properties of the Hyperpolarization-Activated Cation Current, IInternational journal of molecular sciences · 2022Article
- Mitochondria as Therapeutic Targets in Heart Failure.Current heart failure reports · 2022Review
- Late sodium current and calcium homeostasis in arrhythmogenesis.Channels (Austin, Tex.) · 2021Review
- Impact of Sodium-Glucose Co-Transporter 2 Inhibitors on Cardiac Protection.International journal of molecular sciences · 2021Review
- Differential Effect of Three Macrolide Antibiotics on Cardiac Pathology and Electrophysiology in a Myocardial Infarction Rat Model: Influence on Sodium Nav1.5 Channel Expression.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Intracellular NaInternational journal of molecular sciences · 2021Article
- Mechanisms and Perspectives of Sodium-Glucose Co-transporter 2 Inhibitors in Heart Failure.Frontiers in cardiovascular medicine · 2021Review
- SGLT2 inhibitors: mechanisms of cardiovascular benefit beyond glycaemic control.Nature reviews. Cardiology · 2020 · on this mapReview
- Extraglycemic Effects of SGLT2 Inhibitors: A Review of the Evidence.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Review
- Treatments targeting inotropy.European heart journal · 2019Article
- Enhanced Depolarization Drive in Failing Rabbit Ventricular Myocytes: Calcium-Dependent and β-Adrenergic Effects on Late Sodium, L-Type Calcium, and Sodium-Calcium Exchange Currents.Circulation. Arrhythmia and electrophysiology · 2019Article
- SGLT2 Inhibitors Play a Salutary Role in Heart Failure via Modulation of the Mitochondrial Function.Frontiers in cardiovascular medicine · 2019Review
Corrections and comments
- Erratum issuedCorrigendum.2016
Authors and funding
23 authors at 17 institutions in 8 countries.
Funding
Abstract
In February 2014, a group of scientists convened as part of the University of California Davis Cardiovascular Symposium to bring together experimental and mathematical modelling perspectives and discuss points of consensus and controversy on the topic of sodium in the heart. This paper summarizes the topics of presentation and discussion from the symposium, with a focus on the role of aberrant sodium channels and abnormal sodium homeostasis in cardiac arrhythmias and pharmacotherapy from the subcellular scale to the whole heart. Two following papers focus on Na(+) channel structure, function and regulation, and Na(+)/Ca(2+) exchange and Na(+)/K(+) ATPase. The UC Davis Cardiovascular Symposium is a biannual event that aims to bring together leading experts in subfields of cardiovascular biomedicine to focus on topics of importance to the field. The focus on Na(+) in the 2014 symposium stemmed from the multitude of recent studies that point to the importance of maintaining Na(+) homeostasis in the heart, as disruption of homeostatic processes are increasingly identified in cardiac disease states. Understanding how disruption in cardiac Na(+)-based processes leads to derangement in multiple cardiac components at the level of the cell and to then connect these perturbations to emergent behaviour in the heart to cause disease is a critical area of research. The ubiquity of disruption of Na(+) channels and Na(+) homeostasis in cardiac disorders of excitability and mechanics emphasizes the importance of a fundamental understanding of the associated mechanisms and disease processes to ultimately reveal new targets for human therapy.
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.