ArticleFrontiers in physiology2015
A multiscale computational model of spatially resolved calcium cycling in cardiac myocytes: from detailed cleft dynamics to the whole cell concentration profiles.
Article in Frontiers in physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Excitation and mechanical contraction of a 3D cardiomyocyte model.Biophysical journal · 2025Article
- T cell CaFrontiers in immunology · 2023Review
- CaBiophysical journal · 2020Article
- Multiscale Modeling of Dyadic Structure-Function Relation in Ventricular Cardiac Myocytes.Biophysical journal · 2019Article
- NCX-Mediated Subcellular CaBiophysical journal · 2018Article
- 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
- Studying dyadic structure-function relationships: a review of current modeling approaches and new insights into CaClinical Medicine Insights. Cardiology · 2017Article
- Computational cardiology and risk stratification for sudden cardiac death: one of the grand challenges for cardiology in the 21st century.The Journal of physiology · 2016Article
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Authors and funding
5 authors.
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Abstract
Mathematical modeling of excitation-contraction coupling (ECC) in ventricular cardiac myocytes is a multiscale problem, and it is therefore difficult to develop spatially detailed simulation tools. ECC involves gradients on the length scale of 100 nm in dyadic spaces and concentration profiles along the 100 μm of the whole cell, as well as the sub-millisecond time scale of local concentration changes and the change of lumenal Ca(2+) content within tens of seconds. Our concept for a multiscale mathematical model of Ca(2+) -induced Ca(2+) release (CICR) and whole cardiomyocyte electrophysiology incorporates stochastic simulation of individual LC- and RyR-channels, spatially detailed concentration dynamics in dyadic clefts, rabbit membrane potential dynamics, and a system of partial differential equations for myoplasmic and lumenal free Ca(2+) and Ca(2+)-binding molecules in the bulk of the cell. We developed a novel computational approach to resolve the concentration gradients from dyadic space to cell level by using a quasistatic approximation within the dyad and finite element methods for integrating the partial differential equations. We show whole cell Ca(2+)-concentration profiles using three previously published RyR-channel Markov schemes.
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