ReviewCells2021
Remodeling of Ion Channel Trafficking and Cardiac Arrhythmias.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 30 citations in OpenAlex.
- Evolution and paradigms in ion channel and cardiac remodeling: A bibliometric analysis (1979-2024).Medicine · 2026Article
- DENND3-p.R534S disrupts dyadic microdomain architecture to drive potentially pro-arrhythmic calcium and electrophysiologic instability.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 · 2026Article
- High-Throughput Methods for Variant Functional Assessment in Cardiac Disease.Circulation. Genomic and precision medicine · 2026Review
- Article
- Ionic Disorders in Persistent Atrial Fibrillation: Therapeutic Targeting by Plant-Derived Bioactive Compounds.Cardiology research and practice · 2026Review
- Review
- High-throughput screens identify genotype-specific therapeutics for channelopathies.JCI insight · 2025Article
- Ion channel traffic jams: the significance of trafficking deficiency in long QT syndrome.Cell discovery · 2025Review
- A research protocol using ECG monitoring for detection of palpitations-associated arrhythmias in breast cancer survivors.PloS one · 2025Article
- NBQX mediates ventricular fibrillation susceptibility in rat models of anxiety via the Nrf2/HO-1 pathway.Heliyon · 2024Article
- Real-time imaging of axonal membrane protein life cycles.Nature protocols · 2024Review
- X-ray Radiotherapy Impacts Cardiac Dysfunction by Modulating the Sympathetic Nervous System and Calcium Transients.International journal of molecular sciences · 2024Article
- Implications for neutrophils in cardiac arrhythmias.American journal of physiology. Heart and circulatory physiology · 2024Review
- Ion channel trafficking implications in heart failure.Frontiers in cardiovascular medicine · 2024Review
- In silico analysis of the dynamic regulation of cardiac electrophysiology by KThe Journal of physiology · 2023Article
- Human atrial fibrillation and genetic defects in transient outward currents: mechanistic insights from multi-scale computational models.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Article
- Electrical Remodelling in Cardiac Disease.Cells · 2023Article
- Tetramisole is a new IPharmacology research & perspectives · 2022Review
- Novel Perspective of Cardiovascular Diseases: Volume-Regulatory Anion Channels in the Cell Membrane.Membranes · 2022Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Both inherited and acquired cardiac arrhythmias are often associated with the abnormal functional expression of ion channels at the cellular level. The complex machinery that continuously traffics, anchors, organizes, and recycles ion channels at the plasma membrane of a cardiomyocyte appears to be a major source of channel dysfunction during cardiac arrhythmias. This has been well established with the discovery of mutations in the genes encoding several ion channels and ion channel partners during inherited cardiac arrhythmias. Fibrosis, altered myocyte contacts, and post-transcriptional protein changes are common factors that disorganize normal channel trafficking during acquired cardiac arrhythmias. Channel availability, described notably for hERG and K
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.