ArticleBiophysical journal2013
Synchrony of cardiomyocyte Ca(2+) release is controlled by T-tubule organization, SR Ca(2+) content, and ryanodine receptor Ca(2+) sensitivity.
Article in Biophysical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Ryanodine Receptor Staining Identifies Viable Cardiomyocytes in Human and Rabbit Cardiac Tissue Slices.International journal of molecular sciences · 2023Article
- Changes in cellular CaThe Journal of physiology · 2023Article
- Article
- DNA Tension Probes Show that Cardiomyocyte Maturation Is Sensitive to the Piconewton Traction Forces Transmitted by Integrins.ACS nano · 2022Article
- Role of t-tubule remodeling on mechanisms of abnormal calcium release during heart failure development in canine ventricle.American journal of physiology. Heart and circulatory physiology · 2021Article
- The Physiology and Pathophysiology of T-Tubules in the Heart.Frontiers in physiology · 2021Review
- Influence of the tubular network on the characteristics of calcium transients in cardiac myocytes.PloS one · 2020Article
- A Matched-Filter-Based Algorithm for Subcellular Classification of T-System in Cardiac Tissues.Biophysical journal · 2019Article
- Quantitative systems models illuminate arrhythmia mechanisms in heart failure: Role of the NaWiley interdisciplinary reviews. Systems biology and medicine · 2019Review
- Ryanodine receptor dispersion disrupts CaeLife · 2018Article
- Diffusional and Electrical Properties of T-Tubules Are Governed by Their Constrictions and Dilations.Biophysical journal · 2018Article
- Dyadic Plasticity in Cardiomyocytes.Frontiers in physiology · 2018Review
- New Insights in Cardiac Calcium Handling and Excitation-Contraction Coupling.Advances in experimental medicine and biology · 2018Review
- Computational Model of Calcium Signaling in Cardiac Atrial Cells at the Submicron Scale.Frontiers in physiology · 2018Article
- Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection.Cardiovascular diabetology · 2017Review
- T-tubule remodeling and increased heterogeneity of calcium release during the progression to heart failure in intact rat ventricle.Physiological reports · 2017Article
- Electrical defects of the transverse-axial tubular system in cardiac diseases.The Journal of physiology · 2017Review
- 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
- Murine Electrophysiological Models of Cardiac Arrhythmogenesis.Physiological reviews · 2017Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent work has demonstrated that cardiomyocyte Ca(2+)release is desynchronized in several pathological conditions. Loss of Ca(2+) release synchrony has been attributed to t-tubule disruption, but it is unknown if other factors also contribute. We investigated this issue in normal and failing myocytes by integrating experimental data with a mathematical model describing spatiotemporal dynamics of Ca(2+) in the cytosol and sarcoplasmic reticulum (SR). Heart failure development in postinfarction mice was associated with progressive t-tubule disorganization, as quantified by fast-Fourier transforms. Data from fast-Fourier transforms were then incorporated in the model as a dyadic organization index, reflecting the proportion of ryanodine receptors located in dyads. With decreasing dyadic-organization index, the model predicted greater dyssynchrony of Ca(2+) release, which exceeded that observed in experimental line-scan images. Model and experiment were reconciled by reducing the threshold for Ca(2+) release in the model, suggesting that increased RyR sensitivity partially offsets the desynchronizing effects of t-tubule disruption in heart failure. Reducing the magnitude of SR Ca(2+) content and release, whether experimentally by thapsigargin treatment, or in the model, desynchronized the Ca(2+) transient. However, in cardiomyocytes isolated from SERCA2 knockout mice, RyR sensitization offset such effects. A similar interplay between RyR sensitivity and SR content was observed during treatment of myocytes with low-dose caffeine. Initial synchronization of Ca(2+) release during caffeine was reversed as SR content declined due to enhanced RyR leak. Thus, synchrony of cardiomyocyte Ca(2+) release is not only determined by t-tubule organization but also by the interplay between RyR sensitivity and SR Ca(2+) content.
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