ReviewCardiovascular research2013
Alterations in T-tubule and dyad structure in heart disease: challenges and opportunities for computational analyses.
Review in Cardiovascular research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed.
- Natriuretic Peptides as Multisystem Regulators: From Clinical Biomarkers to Therapeutic Targets in Cardio-immunology.Cardiovascular drugs and therapy · 2026Review
- 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
- Ryanodine receptor 2 (RYR2) dysfunction activates the unfolded protein response and perturbs cardiomyocyte maturation.Cardiovascular research · 2023Article
- Basic Research Approaches to Evaluate Cardiac Arrhythmia in Heart Failure and Beyond.Frontiers in physiology · 2022Review
- A Stochastic Spatiotemporal Model of Rat Ventricular Myocyte Calcium Dynamics Demonstrated Necessary Features for Calcium Wave Propagation.Membranes · 2021Article
- Nano-scale morphology of cardiomyocyte t-tubule/sarcoplasmic reticulum junctions revealed by ultra-rapid high-pressure freezing and electron tomography.Journal of molecular and cellular cardiology · 2021Article
- Acute Detubulation of Ventricular Myocytes Amplifies the Inhibitory Effect of Cholinergic Agonist on Intracellular CaFrontiers in physiology · 2021Article
- Structural variability of dyads relates to calcium release in rat ventricular myocytes.Scientific reports · 2020Article
- Arrhythmia mechanisms and spontaneous calcium release: Bi-directional coupling between re-entrant and focal excitation.PLoS computational biology · 2019Article
- Analysis of Cardiac Myocyte Maturation Using CASAAV, a Platform for Rapid Dissection of Cardiac Myocyte Gene Function In Vivo.Circulation research · 2017Review
- Potassium currents in the heart: functional roles in repolarization, arrhythmia and therapeutics.The Journal of physiology · 2017Review
- Ultrastructural Analysis of Self-Associated RyR2s.Biophysical journal · 2016Article
- The ryanodine receptor patchwork: knitting calcium spark dynamics.Biophysical journal · 2014Article
- Calcium and IP3 dynamics in cardiac myocytes: experimental and computational perspectives and approaches.Frontiers in pharmacology · 2014Review
- Imaging T-tubules: dynamic membrane structures for deep functions.Cardiovascular research · 2013Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Compelling recent experimental results make clear that sub-cellular structures are altered in ventricular myocytes during the development of heart failure, in both human samples and diverse experimental models. These alterations can include, but are not limited to, changes in the clusters of sarcoplasmic reticulum (SR) Ca(2+)-release channels, ryanodine receptors, and changes in the average distance between the cell membrane and ryanodine receptor clusters. In this review, we discuss the potential consequences of these structural alterations on the triggering of SR Ca(2+) release during excitation-contraction coupling. In particular, we describe how mathematical models of local SR Ca(2+) release can be used to predict functional changes resulting from diverse modifications that occur in disease states. We review recent studies that have used simulations to understand the consequences of sub-cellular structural changes, and we discuss modifications that will allow for future modelling studies to address unresolved questions. We conclude with a discussion of improvements in both experimental and mathematical modelling techniques that will be required to provide a stronger quantitative understanding of the functional consequences of changes in sub-cellular structure in heart disease.
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Registered trials
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