ArticleAmerican journal of physiology. Heart and circulatory physiology2011
A mathematical model of spontaneous calcium release in cardiac myocytes.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Modeling Calcium Cycling in the Heart: Progress, Pitfalls, and Challenges.Biomolecules · 2022Review
- R-on-T and the initiation of reentry revisited: Integrating old and new concepts.Heart rhythm · 2022Article
- Multi-Scale Computational Modeling of Spatial Calcium Handling From Nanodomain to Whole-Heart: Overview and Perspectives.Frontiers in physiology · 2022Review
- Ventricular Endocardial Tissue Geometry Affects Stimulus Threshold and Effective Refractory Period.Biophysical journal · 2018Article
- Stochastic spontaneous calcium release events and sodium channelopathies promote ventricular arrhythmias.Chaos (Woodbury, N.Y.) · 2017Article
- Stochastic initiation and termination of calcium-mediated triggered activity in cardiac myocytes.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Rabbit-specific computational modelling of ventricular cell electrophysiology: Using populations of models to explore variability in the response to ischemia.Progress in biophysics and molecular biology · 2016Article
- A human ventricular myocyte model with a refined representation of excitation-contraction coupling.Biophysical journal · 2015Article
- Stochastic spontaneous calcium release events trigger premature ventricular complexes by overcoming electrotonic load.Cardiovascular research · 2015Article
- Tissue Structure and Ca2+-Mediated Ectopic Beats.Biomedizinische Technik. Biomedical engineering · 2013Article
- Decoding myocardial Ca²⁺ signals across multiple spatial scales: a role for sensitivity analysis.Journal of molecular and cellular cardiology · 2013Review
- Synchrony of cardiomyocyte Ca(2+) release is controlled by T-tubule organization, SR Ca(2+) content, and ryanodine receptor Ca(2+) sensitivity.Biophysical journal · 2013Article
- Formation of spatially discordant alternans due to fluctuations and diffusion of calcium.PloS one · 2013Article
- Article
- Computational approaches to understand cardiac electrophysiology and arrhythmias.American journal of physiology. Heart and circulatory physiology · 2012Review
- Intracellular Ca2+ waves, afterdepolarizations, and triggered arrhythmias.Cardiovascular research · 2012Article
- Synchronization of early afterdepolarizations and arrhythmogenesis in heterogeneous cardiac tissue models.Biophysical journal · 2012Article
- Criticality in intracellular calcium signaling in cardiac myocytes.Biophysical journal · 2012Article
- The statistics of calcium-mediated focal excitations on a one-dimensional cable.Biophysical journal · 2012Article
- Discrete-state stochastic models of calcium-regulated calcium influx and subspace dynamics are not well-approximated by ODEs that neglect concentration fluctuations.Computational and mathematical methods in medicine · 2012Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
In cardiac myocytes, calcium (Ca) can be released from the sarcoplasmic reticulum independently of Ca influx from voltage-dependent membrane channels. This efflux of Ca, referred to as spontaneous Ca release (SCR), is due to Ryanodine receptor fluctuations, which can induce spontaneous Ca sparks, which propagate to form Ca waves. This release of Ca can then induce delayed after-depolarizations (DADs), which can lead to arrhythmogenic-triggered activity in the heart. However, despite its importance, to date there is no mathematical model of SCR that accounts for experimentally observed features of subcellular Ca. In this article, we present an experimentally based model of SCR that reproduces the timing distribution of spontaneous Ca sparks and key features of the propagation of Ca waves emanating from these spontaneous sparks. We have coupled this model to an ionic model for the rabbit ventricular action potential to simulate SCR within several thousand cells in cardiac tissue. We implement this model to study the formation of an ectopic beat on a cable of cells that exhibit SCR-induced DADs.
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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.