ArticleBiophysical journal2010
Control of Ca2+ release by action potential configuration in normal and failing murine cardiomyocytes.
Article in Biophysical journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Electrophysical cardiac remodeling at the molecular level: Insights into ryanodine receptor activation and calcium-induced calcium release from a stochastic explicit-particle model.Biophysical journal · 2024Article
- Multi-Scale Computational Modeling of Spatial Calcium Handling From Nanodomain to Whole-Heart: Overview and Perspectives.Frontiers in physiology · 2022Review
- Methodology for Cross-Talk Elimination in Simultaneous Voltage and Calcium Optical Mapping Measurements With Semasbestic Wavelengths.Frontiers in physiology · 2022Article
- The Physiology and Pathophysiology of T-Tubules in the Heart.Frontiers in physiology · 2021Review
- Sarcoplasmic Reticulum Calcium Release Is Required for Arrhythmogenesis in the Mouse.Frontiers in physiology · 2021Article
- Applications and Challenges of Machine Learning to Enable Realistic Cellular Simulations.Frontiers in physics · 2020Article
- Regional diastolic dysfunction in post-infarction heart failure: role of local mechanical load and SERCA expression.Cardiovascular research · 2019Article
- Computational Model of Calcium Signaling in Cardiac Atrial Cells at the Submicron Scale.Frontiers in physiology · 2018Article
- Mitochondrial Ca2+ flux modulates spontaneous electrical activity in ventricular cardiomyocytes.PloS one · 2018Article
- Increased passive stiffness promotes diastolic dysfunction despite improved Ca2+ handling during left ventricular concentric hypertrophy.Cardiovascular research · 2017Article
- Bursting dynamics in the normal and failing hearts.Scientific reports · 2017Article
- Regulation of Cardiomyocyte T-Tubular Structure: Opportunities for Therapy.Current heart failure reports · 2017Review
- Studying dyadic structure-function relationships: a review of current modeling approaches and new insights into CaClinical Medicine Insights. Cardiology · 2017Article
- Manipulation of sarcoplasmic reticulum Ca(2+) release in heart failure through mechanical intervention.The Journal of physiology · 2015Review
- Testosterone modulates cardiac contraction and calcium homeostasis: cellular and molecular mechanisms.Biology of sex differences · 2015Review
- Targeting cardiomyocyte Ca2+ homeostasis in heart failure.Current pharmaceutical design · 2015Review
- Alterations in T-tubule and dyad structure in heart disease: challenges and opportunities for computational analyses.Cardiovascular research · 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
- A critical role for Telethonin in regulating t-tubule structure and function in the mammalian heart.Human molecular genetics · 2013Article
- Modelling cardiac calcium sparks in a three-dimensional reconstruction of a calcium release unit.The Journal of physiology · 2012Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Cardiomyocytes from failing hearts exhibit spatially nonuniform or dyssynchronous sarcoplasmic reticulum (SR) Ca(2+) release. We investigated the contribution of action potential (AP) prolongation in mice with congestive heart failure (CHF) after myocardial infarction. AP recordings from CHF and control myocytes were included in a computational model of the dyad, which predicted more dyssynchronous ryanodine receptor opening during stimulation with the CHF AP. This prediction was confirmed in cardiomyocyte experiments, when cells were alternately stimulated by control and CHF AP voltage-clamp waveforms. However, when a train of like APs was used as the voltage stimulus, the control and CHF AP produced a similar Ca(2+) release pattern. In this steady-state condition, greater integrated Ca(2+) entry during the CHF AP lead to increased SR Ca(2+) content. A resulting increase in ryanodine receptor sensitivity synchronized SR Ca(2+) release in the mathematical model, thus offsetting the desynchronizing effects of reduced driving force for Ca(2+) entry. A modest nondyssynchronous prolongation of Ca(2+) release was nevertheless observed during the steady-state CHF AP, which contributed to increased time-to-peak measurements for Ca(2+) transients in failing cells. Thus, dyssynchronous Ca(2+) release in failing mouse myocytes does not result from electrical remodeling, but rather other alterations such as T-tubule reorganization.
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Registered trials
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