ReviewFrontiers in pharmacology2014
Numerical Modeling Calcium and CaMKII Effects in the SA Node.
Review in Frontiers in pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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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
11 citing papers in PubMed, 13 citations in OpenAlex.
- Cardiac pacemaker channel (HCN4) inhibition and atrial arrhythmogenesis after releasing cardiac sympathetic activation.Scientific reports · 2018Trial
- Preserved Autonomic Cardiovascular Regulation With Cardiac Pacemaker Inhibition: A Crossover Trial Using High-Fidelity Cardiovascular Phenotyping.Journal of the American Heart Association · 2016Trial
- Review
- PhysioZoo: A Novel Open Access Platform for Heart Rate Variability Analysis of Mammalian Electrocardiographic Data.Frontiers in physiology · 2018Article
- Age-related pacemaker deterioration is due to impaired intracellular and membrane mechanisms: Insights from numerical modeling.The Journal of general physiology · 2017Article
- Murine Electrophysiological Models of Cardiac Arrhythmogenesis.Physiological reviews · 2017Review
- Enhanced cardiac TBC1D10C expression lowers heart rate and enhances exercise capacity and survival.Scientific reports · 2016Article
- Ion Channels in the Heart.Comprehensive Physiology · 2015Review
- Role of CaMKII in cardiac arrhythmias.Trends in cardiovascular medicine · 2015Review
- Toward a hierarchy of mechanisms in CaMKII-mediated arrhythmia.Frontiers in pharmacology · 2014Review
- CaMKII comes of age in cardiac health and disease.Frontiers in pharmacology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sinoatrial node (SAN) is the primary heart pacemaker which initiates each heartbeat under normal conditions. Numerous experimental data have demonstrated that Ca(2+-) and CaMKII-dependent processes are crucially important for regulation of SAN cells. However, specific mechanisms of this regulation and their relative contribution to pacemaker function remain mainly unknown. Our review summarizes available data and existing numerical modeling approaches to understand Ca(2+) and CaMKII effects on the SAN. Data interpretation and future directions to address the problem are given within the coupled-clock theory, i.e., a modern view on the cardiac pacemaker cell function generated by a system of sarcolemmal and intracellular proteins.
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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.