ArticleBiophysical journal2017
Mechanism for Triggered Waves in Atrial Myocytes.
Article in Biophysical journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- APD restitution controls arrhythmia emergence in cardiac tissue with RyR2 dysfunction.The Journal of physiology · 2026Article
- Mechanism of Arrhythmogenesis Driven by Early After Depolarizations in Cardiac Tissue.PLoS computational biology · 2025Article
- Mechanisms of spontaneous CaThe Journal of physiology · 2023Article
- Partial and complete loss of myosin binding protein H-like cause cardiac conduction defects.Journal of molecular and cellular cardiology · 2022Article
- Review
- Voltage-mediated mechanism for calcium wave synchronization and arrhythmogenesis in atrial tissue.Biophysical journal · 2022Article
- Multi-Scale Computational Modeling of Spatial Calcium Handling From Nanodomain to Whole-Heart: Overview and Perspectives.Frontiers in physiology · 2022Review
- Effect of Occurrence of Lamin A/C (Frontiers in cardiovascular medicine · 2022Article
- Triggered CaCirculation. Arrhythmia and electrophysiology · 2020Article
- Remodeling Promotes Proarrhythmic Disruption of Calcium Homeostasis in Failing Atrial Myocytes.Biophysical journal · 2020Article
- Region-specific parasympathetic nerve remodeling in the left atrium contributes to creation of a vulnerable substrate for atrial fibrillation.JCI insight · 2019Article
- Synchronization of Triggered Waves in Atrial Tissue.Biophysical journal · 2018Article
- Alcoholism: A Multi-Systemic Cellular Insult to Organs.International journal of environmental research and public health · 2018Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Excitation-contraction coupling in atrial cells is mediated by calcium (Ca) signaling between L-type Ca channels and Ryanodine receptors that occurs mainly at the cell boundary. This unique architecture dictates essential aspects of Ca signaling under both normal and diseased conditions. In this study we apply laser scanning confocal microscopy, along with an experimentally based computational model, to understand the Ca cycling dynamics of an atrial cell subjected to rapid pacing. Our main finding is that when an atrial cell is paced under Ca overload conditions, Ca waves can then nucleate on the cell boundary and propagate to the cell interior. These propagating Ca waves are referred to as "triggered waves" because they are initiated by L-type Ca channel openings during the action potential. These excitations are distinct from spontaneous Ca waves originating from random fluctuations of Ryanodine receptor channels, and which occur after much longer waiting times. Furthermore, we argue that the onset of these triggered waves is a highly nonlinear function of the sarcoplasmic reticulum Ca load. This strong nonlinearity leads to aperiodic response of Ca at rapid pacing rates that is caused by the complex interplay between paced Ca release and triggered waves. We argue further that this feature of atrial cells leads to dynamic instabilities that may underlie atrial arrhythmias. These studies will serve as a starting point to explore the nonlinear dynamics of atrial cells and will yield insights into the trigger and maintenance of atrial fibrillation.
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