ArticleThe Journal of physiology2010
Local Ca2+ releases enable rapid heart rates in developing cardiomyocytes.
Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 27 citations in OpenAlex.
- Gradient-based parameter optimization method to determine membrane ionic current composition in human induced pluripotent stem cell-derived cardiomyocytes.Scientific reports · 2022Trial
- Injection of IFrontiers in physiology · 2023Article
- Building blocks of microphysiological system to model physiology and pathophysiology of human heart.Frontiers in physiology · 2023Review
- Computational modeling of aberrant electrical activity following remuscularization with intramyocardially injected pluripotent stem cell-derived cardiomyocytes.Journal of molecular and cellular cardiology · 2022Article
- The Physiology and Pathophysiology of T-Tubules in the Heart.Frontiers in physiology · 2021Review
- IP3R-Mediated Compensatory Mechanism for Calcium Handling in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes With Cardiac Ryanodine Receptor Deficiency.Frontiers in cell and developmental biology · 2020Article
- Adipose tissue derived mesenchymal stem cells are better respondents to TGFβ1 for in vitro generation of cardiomyocyte-like cells.Molecular and cellular biochemistry · 2019Article
- Nexilin Is a New Component of Junctional Membrane Complexes Required for Cardiac T-Tubule Formation.Circulation · 2019Article
- Structural Immaturity of Human iPSC-Derived Cardiomyocytes:Frontiers in physiology · 2018Article
- Sarcoplasmic reticulum CaPhysiological reports · 2018Article
- Dyadic Plasticity in Cardiomyocytes.Frontiers in physiology · 2018Review
- Regulation of Cardiomyocyte T-Tubular Structure: Opportunities for Therapy.Current heart failure reports · 2017Review
- Vascular Endothelial Growth Factor-B Induces a Distinct Electrophysiological Phenotype in Mouse Heart.Frontiers in physiology · 2017Article
- Peroxisome proliferator-activated receptor-γ coactivator 1 α1 induces a cardiac excitation-contraction coupling phenotype without metabolic remodelling.The Journal of physiology · 2016Article
- Calcium signalling in developing cardiomyocytes: implications for model systems and disease.The Journal of physiology · 2015Review
- Arrhythmogenic calmodulin mutations disrupt intracellular cardiomyocyte Ca2+ regulation by distinct mechanisms.Journal of the American Heart Association · 2014Article
- Small molecules enable cardiac reprogramming of mouse fibroblasts with a single factor, Oct4.Cell reports · 2014Article
- Impact of sarcoplasmic reticulum calcium release on calcium dynamics and action potential morphology in human atrial myocytes: a computational study.PLoS computational biology · 2011Article
- Calcium channel blockade in embryonic cardiac progenitor cells disrupts normal cardiac cell differentiation.Stem cells and development · 2010Article
- Ca2+ on the move: what is better - fire and forget, or fire-diffuse-fire?The Journal of physiology · 2010Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ability to generate homogeneous intracellular Ca(2+) oscillations at high frequency is the basis of the rhythmic contractions of mammalian cardiac myocytes. While the specific mechanisms and structures enabling homogeneous high-frequency Ca(2+) signals in adult cardiomyocytes are well characterized, it is not known how these kind of Ca(2+) signals are produced in developing cardiomyocytes. Here we investigated the mechanisms reducing spatial and temporal heterogeneity of cytosolic Ca(2+) signals in mouse embryonic ventricular cardiomyocytes. We show that in developing cardiomyocytes the propagating Ca(2+) signals are amplified in cytosol by local Ca(2+) releases. Local releases are based on regular 3-D sarcoplasmic reticulum (SR) structures containing SR Ca(2+) uptake ATPases (SERCA) and Ca(2+) release channels (ryanodine receptors, RyRs) at regular intervals throughout the cytosol. By evoking [Ca(2+)](i)-induced Ca(2+) sparks, the local release sites promote a 3-fold increase in the cytosolic Ca(2+) propagation speed. We further demonstrate by mathematical modelling that without these local release sites the developing cardiomyocytes lose their ability to generate homogeneous global Ca(2+) signals at a sufficiently high frequency. The mechanism described here is robust and indispensable for normal mammalian cardiomyocyte function from the first heartbeats during the early embryonic phase till terminal differentiation after birth. These results suggest that local cytosolic Ca(2+) releases are indispensable for normal cardiomyocyte development and function of developing heart.
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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.