ArticleJournal of molecular and cellular cardiology2012
Calsequestrin 2 deletion shortens the refractoriness of Ca²⁺ release and reduces rate-dependent Ca²⁺-alternans in intact mouse hearts.
Article in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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56 citing papers in PubMed, 79 citations in OpenAlex.
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- Thermal modulation of epicardial Ca2+ dynamics uncovers molecular mechanisms of Ca2+ alternans.The Journal of general physiology · 2021Article
- Role of Reduced Sarco-Endoplasmic Reticulum CaFrontiers in physiology · 2021Article
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- CaCell calcium · 2020Review
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- Phase 1 repolarization rate defines CaThe Journal of general physiology · 2019Article
- Action potential shortening rescues atrial calcium alternans.The Journal of physiology · 2019Article
- Open-Source Multiparametric Optocardiography.Scientific reports · 2019Article
- Transmural Autonomic Regulation of Cardiac Contractility at the Intact Heart Level.Frontiers in physiology · 2019Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Calsequestrin (Casq2) is a low affinity Ca(2+)-binding protein located in sarcoplasmic reticulum (SR) of cardiac myocytes. Casq2 acts as a Ca(2+) buffer regulating free Ca(2+) concentration in the SR lumen and plays a significant role in the regulation of Ca(2+) release from this intracellular organelle. In addition, there is experimental evidence supporting the hypothesis that Casq2 also modulates the activity of the cardiac Ca(2+) release channels, ryanodine receptors (RyR2). In this study, Casq2 knockout mice (Casq2-/-) were used as a model to evaluate the effects of the Casq2 on the cytosolic and intra-SR Ca(2+) dynamics, and the electrical activity in the ventricular epicardial layer of intact beating hearts. Casq2-/- mice have accelerated intra-SR Ca(2+) refilling kinetics (76 ± 22 vs. 136.5 ± 15 ms) and a reduced refractoriness of Ca(2+) release (182 ± 32 ms Casq2+/+ and 111 ± 22 ms Casq2-/- ). In addition, mice display reduced Ca(2+) alternans (67% decline in the amplitude of Ca(2+) alternans at 7 Hz, 21oC) and less T-wave alternans at the electrocardiographic level. The results presented in this paper support the idea of Casq2 acting both as a buffer and a direct regulator of the Ca(2+) release process. Finally, we propose that alterations in Ca(2+) release refractoriness shown here could explain the relationship between Casq2 function and an increase in the risk for ventricular arrhythmias.
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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.