ArticleAnnals of the New York Academy of Sciences2004
Modeling the actions of beta-adrenergic signaling on excitation--contraction coupling processes.
Article in Annals of the New York Academy of Sciences, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 29 citations in OpenAlex.
- A model of β-adrenergic stimulation in human ventricular cells for tissue-scale simulations of sympathetically modulated tachycardias.The Journal of physiology · 2026Article
- Review
- Estimating the probability of early afterdepolarizations and predicting arrhythmic risk associated with long QT syndrome type 1 mutations.Biophysical journal · 2023Article
- Estimating ectopic beat probability with simplified statistical models that account for experimental uncertainty.PLoS computational biology · 2021Article
- Estimating the probabilities of rare arrhythmic events in multiscale computational models of cardiac cells and tissue.PLoS computational biology · 2017Article
- Mechanisms of the cyclic nucleotide cross-talk signaling network in cardiac L-type calcium channel regulation.Journal of molecular and cellular cardiology · 2017Article
- The force-frequency relationship: insights from mathematical modeling.Advances in physiology education · 2013Review
- Cardiac myocytes and local signaling in nano-domains.Progress in biophysics and molecular biology · 2011Review
- A mathematical model of action potentials of mouse sinoatrial node cells with molecular bases.American journal of physiology. Heart and circulatory physiology · 2011Article
- Computational models reduce complexity and accelerate insight into cardiac signaling networks.Circulation research · 2011Review
- Integrative systems models of cardiac excitation-contraction coupling.Circulation research · 2011Review
- Models of cardiac excitation-contraction coupling in ventricular myocytes.Mathematical biosciences · 2010Review
- From mitochondrial ion channels to arrhythmias in the heart: computational techniques to bridge the spatio-temporal scales.Philosophical transactions. Series A, Mathematical, physical, and engineering sciences · 2008Review
- Using models of the myocyte for functional interpretation of cardiac proteomic data.The Journal of physiology · 2005Review
- The role of stochastic and modal gating of cardiac L-type Ca2+ channels on early after-depolarizations.Biophysical journal · 2005Article
- Integrative modeling of the cardiac ventricular myocyte.Wiley interdisciplinary reviews. Systems biology and medicineReview
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
Activation of the beta-adrenergic (beta-AR) signaling pathway enhances cardiac function through protein kinase A (PKA)-mediated phosphorylation of target proteins involved in the process of excitation-contraction (EC) coupling. Experimental studies of the effects of beta-AR stimulation on EC coupling have yielded complex results, including increased, decreased, or unchanged EC coupling gain. In this study, we extend a previously developed model of the canine ventricular myocyte describing local control of sarcoplasmic reticulum (SR) calcium (Ca(2+)) release to include the effects of beta-AR stimulation. Incorporation of phosphorylation-dependent effects on model membrane currents and Ca(2+)-cycling proteins yields changes of action potential (AP) and Ca(2+) transients in agreement with those measured experimentally in response to the nonspecific beta-AR agonist isoproterenol (ISO). The model reproduces experimentally observed alterations in EC coupling gain in response to beta-AR agonists and predicts the specific roles of L-type Ca(2+) channel (LCC) and SR Ca(2+) release channel phosphorylation in altering the amplitude and shape of the EC coupling gain function. The model also indicates that factors that promote mode 2 gating of LCCs, such as beta-AR stimulation or activation of the Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), may increase the probability of occurrence of early after-depolarizations (EADs), due to the random, long-duration opening of LCC gating in mode 2.
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.