ArticleBiophysical journal2004
A mathematical analysis of the generation and termination of calcium sparks.
Article in Biophysical journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed.
- Multi-Scale Computational Modeling of Spatial Calcium Handling From Nanodomain to Whole-Heart: Overview and Perspectives.Frontiers in physiology · 2022Review
- Image-Driven Modeling of Nanoscopic Cardiac Function: Where Have We Come From, and Where Are We Going?Frontiers in physiology · 2022Review
- Mechanisms Underlying Spontaneous Action Potential Generation Induced by Catecholamine in Pulmonary Vein Cardiomyocytes: A Simulation Study.International journal of molecular sciences · 2019Article
- Quenching the spark: Termination of CICR in the submicroscopic space of the dyad.The Journal of general physiology · 2017Review
- 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
- Long-Lasting Sparks: Multi-Metastability and Release Competition in the Calcium Release Unit Network.PLoS computational biology · 2016Article
- Cytosolic Ca²⁺ buffering determines the intra-SR Ca²⁺ concentration at which cardiac Ca²⁺ sparks terminate.Cell calcium · 2015Article
- A human ventricular myocyte model with a refined representation of excitation-contraction coupling.Biophysical journal · 2015Article
- Nonlinear and Stochastic Dynamics in the Heart.Physics reports · 2014Article
- Termination of calcium puffs and coupled closings of inositol trisphosphate receptor channels.Cell calcium · 2014Article
- The influence of Ca²⁺ buffers on free [Ca²⁺] fluctuations and the effective volume of Ca²⁺ microdomains.Biophysical journal · 2014Article
- Life and death of a cardiac calcium spark.The Journal of general physiology · 2013Article
- Mechanism of calsequestrin regulation of single cardiac ryanodine receptor in normal and pathological conditions.The Journal of general physiology · 2013Article
- Pernicious attrition and inter-RyR2 CICR current control in cardiac muscle.Journal of molecular and cellular cardiology · 2013Review
- Article
- Ca²⁺-induced delayed afterdepolarizations are triggered by dyadic subspace Ca2²⁺ affirming that increasing SERCA reduces aftercontractions.American journal of physiology. Heart and circulatory physiology · 2011Article
- Identification of changes in the functional profile of the cardiac ryanodine receptor caused by the coupled gating phenomenon.The Journal of membrane biology · 2010Article
- Alteration of sarcoplasmic reticulum Ca2+ release termination by ryanodine receptor sensitization and in heart failure.The Journal of physiology · 2009Article
- Termination of cardiac Ca2+ sparks: role of intra-SR [Ca2+], release flux, and intra-SR Ca2+ diffusion.Circulation research · 2008Article
- Calsequestrin-mediated mechanism for cellular calcium transient alternans.Biophysical journal · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium sparks are local regenerative releases of Ca(2+) from a cluster of ryanodine receptors on the sarcoplasmic reticulum. During excitation-contraction coupling in cardiac cells, Ca(2+) sparks are triggered by Ca(2+) entering the cell via the T-tubules (Ca(2+)-induced Ca(2+) release). However under conditions of calcium overload, Ca(2+) sparks can be triggered spontaneously. The exact process by which Ca(2+) sparks terminate is still an open question, although both deterministic and stochastic processes are likely to be important. In this article, asymptotic methods are used to analyze a single Ca(2+) spark model, which includes both deterministic and stochastic biophysical mechanisms. The analysis calculates both spark frequencies and spark duration distributions, and shows under what circumstances stochastic transitions are important. Additionally, a model of the coupling of the release channels via the FK-binding protein is analyzed.
Indexed as
Identifiers
What OpenQuestion holds
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.