ArticleBiophysical journal2011
Multiscale modeling of calcium cycling in cardiac ventricular myocyte: macroscopic consequences of microscopic dyadic function.
Article in Biophysical journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.
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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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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- DENND3-p.R534S disrupts dyadic microdomain architecture to drive potentially pro-arrhythmic calcium and electrophysiologic instability.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026Article
- Role of ryanodine receptor cooperativity in CaThe Journal of physiology · 2024Article
- Diversity of cells and signals in the cardiovascular system.The Journal of physiology · 2023Article
- Modeling Calcium Cycling in the Heart: Progress, Pitfalls, and Challenges.Biomolecules · 2022Review
- Multi-Scale Computational Modeling of Spatial Calcium Handling From Nanodomain to Whole-Heart: Overview and Perspectives.Frontiers in physiology · 2022Review
- CaBiophysical journal · 2020Article
- Stochastic spontaneous calcium release events and sodium channelopathies promote ventricular arrhythmias.Chaos (Woodbury, N.Y.) · 2017Article
- A computational model of spatio-temporal cardiac intracellular calcium handling with realistic structure and spatial flux distribution from sarcoplasmic reticulum and t-tubule reconstructions.PLoS computational biology · 2017Article
- Multiscale modeling methods in biomechanics.Wiley interdisciplinary reviews. Systems biology and medicine · 2017Review
- 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
- Long-Lasting Sparks: Multi-Metastability and Release Competition in the Calcium Release Unit Network.PLoS computational biology · 2016Article
- Stochastic spontaneous calcium release events trigger premature ventricular complexes by overcoming electrotonic load.Cardiovascular research · 2015Article
- Superresolution modeling of calcium release in the heart.Biophysical journal · 2014Article
- Images as drivers of progress in cardiac computational modelling.Progress in biophysics and molecular biology · 2014Review
- Alterations in T-tubule and dyad structure in heart disease: challenges and opportunities for computational analyses.Cardiovascular research · 2013Review
- Decoding myocardial Ca²⁺ signals across multiple spatial scales: a role for sensitivity analysis.Journal of molecular and cellular cardiology · 2013Review
- Parameter sensitivity analysis of stochastic models provides insights into cardiac calcium sparks.Biophysical journal · 2013Article
- Determinants of beat-to-beat variability of repolarization duration in the canine ventricular myocyte: a computational analysis.PLoS computational biology · 2013Article
- Computational approaches to understand cardiac electrophysiology and arrhythmias.American journal of physiology. Heart and circulatory physiology · 2012Review
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In cardiac ventricular myocytes, calcium (Ca) release occurs at distinct structures (dyads) along t-tubules, where L-type Ca channels (LCCs) appose sarcoplasmic reticulum (SR) Ca release channels (RyR2s). We developed a model of the cardiac ventricular myocyte that simulates local stochastic Ca release processes. At the local Ca release level, the model reproduces Ca spark properties. At the whole-cell level, the model reproduces the action potential, Ca currents, and Ca transients. Changes in microscopic dyadic properties (e.g., during detubulation in heart failure) affect whole-cell behavior in complex ways, which we investigated by simulating changes in the dyadic volume and number of LCCs/RyR2s in the dyad, and effects of calsequestrin (CSQN) as a Ca buffer (CSQN buffer) or a luminal Ca sensor (CSQN regulator). We obtained the following results: 1), Increased dyadic volume and reduced LCCs/RyR2s decrease excitation-contraction coupling gain and cause asynchrony of SR Ca release, and interdyad coupling partially compensates for the reduced synchrony. 2), Impaired CSQN buffer depresses Ca transients without affecting the synchrony of SR Ca release. 3), When CSQN regulator function is impaired, interdyad coupling augments diastolic Ca release activity to form Ca waves and long-lasting Ca release events.
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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.