ArticleBiophysical journal2012
CaMKIIδC slows [Ca]i decline in cardiac myocytes by promoting Ca sparks.
Article in Biophysical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Compromised repolarization reserve in a murine model of catecholaminergic polymorphic ventricular tachycardia caused by RyR2-R420Q mutation.Journal of molecular and cellular cardiology · 2025Article
- CaMKII-Dependent Contractile Dysfunction and Pro-Arrhythmic Activity in a Mouse Model of Obstructive Sleep Apnea.Antioxidants (Basel, Switzerland) · 2023Article
- Cardiac function, structural, and electrical remodeling by microgravity exposure.American journal of physiology. Heart and circulatory physiology · 2023Review
- Review
- The oxidation-resistant CaMKII-MM281/282VV mutation does not prevent arrhythmias in CPVT1.Physiological reports · 2021Article
- JNK2, a Newly-Identified SERCA2 Enhancer, Augments an Arrhythmic [CaCirculation research · 2021Article
- Hyperglycemia Acutely Increases Cytosolic Reactive Oxygen Species viaCirculation research · 2020Article
- The Control of Diastolic Calcium in the Heart: Basic Mechanisms and Functional Implications.Circulation research · 2020Review
- Unique CaInternational journal of molecular sciences · 2018Review
- Computational modeling of amylin-induced calcium dysregulation in rat ventricular cardiomyocytes.Cell calcium · 2018Article
- Stress Signaling JNK2 Crosstalk With CaMKII Underlies Enhanced Atrial Arrhythmogenesis.Circulation research · 2018Article
- Late CaCirculation research · 2018Article
- Arrhythmogenic Mechanisms in Heart Failure: Linking β-Adrenergic Stimulation, Stretch, and Calcium.Frontiers in physiology · 2018Review
- Calcium-Mediated Oscillation in Membrane Potentials and Atrial-Triggered Activity in Atrial Cells of Casq2Frontiers in physiology · 2018Article
- Ambiguous interactions between diastolic and SR CaThe Journal of general physiology · 2017Review
- Calcium and Excitation-Contraction Coupling in the Heart.Circulation research · 2017Review
- Biphasic decay of the Ca transient results from increased sarcoplasmic reticulum Ca leak.The Journal of physiology · 2016Article
- Oxidative stress and ca(2+) release events in mouse cardiomyocytes.Biophysical journal · 2014Article
- Cardiac myocyte Z-line calmodulin is mainly RyR2-bound, and reduction is arrhythmogenic and occurs in heart failure.Circulation research · 2014Article
- The arrhythmogenic consequences of increasing late INa in the cardiomyocyte.Cardiovascular research · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Acute activation of calcium/calmodulin-dependent protein kinase (CaMKII) in permeabilized phospholamban knockout (PLN-KO) mouse myocytes phosphorylates ryanodine receptors (RyRs) and activates spontaneous local sarcoplasmic reticulum (SR) Ca release events (Ca sparks) even at constant SR Ca load. To assess how CaMKII regulates SR Ca release in intact myocytes (independent of SR Ca content changes or PLN effects), we compared Ca sparks in PLN-KO versus mice, which also have transgenic cardiac overexpression of CaMKIIδC in the PLN-KO background (KO/TG). Compared with PLN-KO mice, these KO/TG cardiomyocytes exhibited 1), increased twitch Ca transient and fractional release (both by ∼35%), but unaltered SR Ca load; 2), increased resting Ca spark frequency (300%) despite a lower diastolic [Ca]i, which also slowed twitch [Ca]i decline (suggesting CaMKII-dependent RyR Ca sensitization); 3), elevated Ca spark amplitude and rate of Ca release (which might indicate that more RyR channels participate in a single spark); 4), prolonged Ca spark rise time (which implies that CaMKII either delays RyR closure or prolongs the time when openings can occur); 5), more frequent repetitive sparks at single release sites. Analysis of repetitive sparks from individual Ca release sites indicates that CaMKII enhanced RyR Ca sensitivity, but did not change the time course of SR Ca refilling. These results demonstrate that there are dramatic CaMKII-mediated effects on RyR Ca release that occur via regulation of both RyR activation and termination processes.
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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.