ReviewFrontiers in physiology2024
Cardiac arrhythmogenesis: roles of ion channels and their functional modification.
Review in Frontiers in physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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Who cites it
23 citing papers in PubMed, 20 citations in OpenAlex.
- Integrated Multi-Cohort Transcriptomic Analysis Reveals Molecular Networks and Signaling Pathway Landscape of Aconitine-Induced Cardiotoxicity and Myocardial Injury.Cardiovascular toxicology · 2026Article
- Evolution and paradigms in ion channel and cardiac remodeling: A bibliometric analysis (1979-2024).Medicine · 2026Article
- Revising NHE-1: From Cardiac Homeostasis to Heart Failure and Future Drug Development.Cell biochemistry and function · 2026Review
- From Ischemic Injury to Arrhythmogenic Substrate: Molecular and Histopathological Insights into Post-Infarction Sudden Cardiac Death.Life (Basel, Switzerland) · 2026Review
- Predictive utility of the baseline Tp-e interval for early arrhythmic events in acute myocardial infarction: A cohort study.The Journal of international medical research · 2026Article
- Review
- Single Antenatal Exposure to Ciclesonide Reduces Long-Term Cardiac Structural and Functional Alterations Compared to Currently Approved Synthetic Corticosteroids.Research square · 2026Article
- Review
- Causal AI in Cardiac Arrhythmia: From Pattern Recognition to Mechanistic Insight.Clinical cardiology · 2026Review
- Salivary Redox Biomarkers as a Non-Invasive Research Framework for Exploring Redox-Related Cardiac Electrical Vulnerability in Sudden Unexplained Cardiac Death: A Mechanistic and Narrative Review.Medicina (Kaunas, Lithuania) · 2026Review
- Mechanical Modeling of Cardiac Fibrosis With Explicit Spatial Representation of Cellular Structure and Collagen Alignment.Journal of biomechanical engineering · 2026Article
- Predictive value of the monocyte-to-high-density lipoprotein cholesterol ratio in atrial fibrillation: a meta-analysis.Frontiers in cardiovascular medicine · 2026Review
- Multifunctional nanoplatforms for optic nerve regeneration integrating anti-inflammatory, epigenetic, and ionic mechanisms with emerging artificial intelligence technologies.Cell biology and toxicology · 2025Review
- Review
- Therapeutic Challenges in Total Situs Inversus Associated with Sick Sinus Syndrome, Ventricular Arrhythmias, and Heart Failure with Preserved Ejection Fraction: Narrative Review and Case Report.Journal of cardiovascular development and disease · 2025Review
- Role of ionic electrodiffusion and ephaptic coupling in cardiac dynamics.Biophysical journal · 2025Article
- Consequences of Right Heart Disease for Cardiac Electrophysiology and Arrhythmias: Cellular and Structural Mechanisms.CJC open · 2025Review
- Modulation of Redox-Sensitive Cardiac Ion Channels.Antioxidants (Basel, Switzerland) · 2025Review
- Inflammasome Signaling in Cardiac Arrhythmias: Linking Inflammation, Fibrosis, and Electrical Remodeling.International journal of molecular sciences · 2025Review
- Compound Testing of Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes Using Multi-Well Microelectrode Arrays.Methods in molecular biology (Clifton, N.J.) · 2025Article
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 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac arrhythmias cause significant morbidity and mortality and pose a major public health problem. They arise from disruptions in the normally orderly propagation of cardiac electrophysiological activation and recovery through successive cardiomyocytes in the heart. They reflect abnormalities in automaticity, initiation, conduction, or recovery in cardiomyocyte excitation. The latter properties are dependent on surface membrane electrophysiological mechanisms underlying the cardiac action potential. Their disruption results from spatial or temporal instabilities and heterogeneities in the generation and propagation of cellular excitation. These arise from abnormal function in their underlying surface membrane, ion channels, and transporters, as well as the interactions between them. The latter, in turn, form common regulatory targets for the hierarchical network of diverse signaling mechanisms reviewed here. In addition to direct
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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.