ArticleJournal of molecular and cellular cardiology2015
Ca2+ Sparks and Ca2+ waves are the subcellular events underlying Ca2+ overload during ischemia and reperfusion in perfused intact hearts.
Article in Journal of molecular and cellular cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- Sex differences in mitochondrial CaJournal of molecular and cellular cardiology · 2026Article
- Disturbed Repolarization-Relaxation Coupling During Acute Myocardial Ischemia Permits Systolic Mechano-Arrhythmogenesis.Circulation research · 2025Article
- Macrophage-mediated IL-6 signaling drives ryanodine receptor-2 calcium leak in postoperative atrial fibrillation.The Journal of clinical investigation · 2025Article
- Enhanced Late IInternational journal of molecular sciences · 2024Article
- The adipose-neural axis is involved in epicardial adipose tissue-related cardiac arrhythmias.Cell reports. Medicine · 2024Article
- Autonomic Regulation of the Goldfish Intact Heart.Frontiers in physiology · 2022Article
- Activation of CCL21-GPR174/CCR7 on cardiac fibroblasts underlies myocardial ischemia/reperfusion injury.Frontiers in genetics · 2022Article
- Quercetin Protects H9c2 Cardiomyocytes against Oxygen-Glucose Deprivation/Reoxygenation-Induced Oxidative Stress and Mitochondrial Apoptosis by Regulating the ERK1/2/DRP1 Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Long Noncoding RNAs in Myocardial Ischemia-Reperfusion Injury.Oxidative medicine and cellular longevity · 2021Review
- Heat Shock Protein 70 Protects the Heart from Ischemia/Reperfusion Injury through Inhibition of p38 MAPK Signaling.Oxidative medicine and cellular longevity · 2020Article
- Ischemia Enhances the Acute Stretch-Induced Increase in Calcium Spark Rate in Ventricular Myocytes.Frontiers in physiology · 2020Article
- Phase 1 repolarization rate defines CaThe Journal of general physiology · 2019Article
- Ablation of phospholamban rescues reperfusion arrhythmias but exacerbates myocardium infarction in hearts with Ca2+/calmodulin kinase II constitutive phosphorylation of ryanodine receptors.Cardiovascular research · 2019Article
- Transmural Autonomic Regulation of Cardiac Contractility at the Intact Heart Level.Frontiers in physiology · 2019Article
- Unbalance Between Sarcoplasmic Reticulum CaFrontiers in physiology · 2019Review
- Dexmedetomidine protects H9c2 cardiomyocytes against oxygen-glucose deprivation/reoxygenation-induced intracellular calcium overload and apoptosis through regulating FKBP12.6/RyR2 signaling.Drug design, development and therapy · 2019Article
- Local Field Fluorescence Microscopy: Imaging Cellular Signals in Intact Hearts.Journal of visualized experiments : JoVE · 2017Article
- Metabolic inhibition reduces cardiac L-type Ca2+ channel current due to acidification caused by ATP hydrolysis.PloS one · 2017Article
- Phospholamban ablation rescues the enhanced propensity to arrhythmias of mice with CaMKII-constitutive phosphorylation of RyR2 at site S2814.The Journal of physiology · 2016Article
- A technical review of optical mapping of intracellular calcium within myocardial tissue.American journal of physiology. Heart and circulatory physiology · 2016Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Abnormal intracellular Ca(2+) cycling plays a key role in cardiac dysfunction, particularly during the setting of ischemia/reperfusion (I/R). During ischemia, there is an increase in cytosolic and sarcoplasmic reticulum (SR) Ca(2+). At the onset of reperfusion, there is a transient and abrupt increase in cytosolic Ca(2++), which occurs timely associated with reperfusion arrhythmias. However, little is known about the subcellular dynamics of Ca(2+) increase during I/R, and a possible role of the SR as a mechanism underlying this increase has been previously overlooked. The aim of the present work is to test two main hypotheses: (1) An increase diastolic Ca(2+) sparks frequency (cspf) constitutes a mayor substrate for the ischemia-induced diastolic Ca(2+) increase; (2) an increase in cytosolic Ca(2+) pro-arrhythmogenic events (Ca(2+) waves), mediates the abrupt diastolic Ca(2+) rise at the onset of reperfusion. We used confocal microscopy on mouse intact hearts loaded with Fluo-4. Hearts were submitted to global I/R (12/30 min) to assess epicardial Ca(2+) sparks in the whole heart. Intact heart sparks were faster than in isolated myocytes whereas cspf was not different. During ischemia, cspf significantly increased relative to preischemia (2.07±0.33 vs. 1.13±0.20 sp/s/100 μm, n=29/34, 7 hearts). Reperfusion significantly changed Ca(2+) sparks kinetics, by prolonging Ca(2+) sparks rise time and decreased cspf. However, it significantly increased Ca(2+) wave frequency relative to ischemia (0.71±0.14 vs. 0.38±0.06 w/s/100 μm, n=32/33, 7 hearts). The results show for the first time the assessment of intact perfused heart Ca(2+) sparks and provides direct evidence of increased Ca(2+) sparks in ischemia that transform into Ca(2+) waves during reperfusion. These waves may constitute a main trigger for reperfusion arrhythmias.
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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.