ArticleCirculation research2010
Alterations of L-type calcium current and cardiac function in CaMKII{delta} knockout mice.
Article in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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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
28 citing papers in PubMed, 53 citations in OpenAlex.
- CaCells · 2024Review
- Reduced O-GlcNAcylation diminishes cardiomyocyte CaJournal of molecular and cellular cardiology · 2023Article
- L-type CaPhysiological reports · 2022Article
- GRK5 Controls SAP97-Dependent Cardiotoxic βCirculation research · 2020Article
- Article
- Regulation of cardiovascular calcium channel activity by post-translational modifications or interacting proteins.Pflugers Archiv : European journal of physiology · 2020Review
- MicroRNA-145 Protects against Myocardial Ischemia Reperfusion Injury via CaMKII-Mediated Antiapoptotic and Anti-Inflammatory Pathways.Oxidative medicine and cellular longevity · 2019Article
- Unique CaInternational journal of molecular sciences · 2018Review
- Altered CaFrontiers in physiology · 2018Article
- Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes.Journal of visualized experiments : JoVE · 2017Article
- CaMKII-dependent phosphorylation regulates basal cardiac pacemaker function via modulation of local Ca2+ releases.American journal of physiology. Heart and circulatory physiology · 2016Article
- Time-dependent evolution of functional vs. remodeling signaling in induced pluripotent stem cell-derived cardiomyocytes and induced maturation with biomechanical stimulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Recent advances in understanding cardiac contractility in health and disease.F1000Research · 2016Review
- CaMKII-dependent myofilament Ca2+ desensitization contributes to the frequency-dependent acceleration of relaxation.Cell calcium · 2015Article
- CaMKIIδ mediates β-adrenergic effects on RyR2 phosphorylation and SR Ca(2+) leak and the pathophysiological response to chronic β-adrenergic stimulation.Journal of molecular and cellular cardiology · 2015Article
- Ca(2+) current facilitation is CaMKII-dependent and has arrhythmogenic consequences.Frontiers in pharmacology · 2014Review
- CaMKII in sinoatrial node physiology and dysfunction.Frontiers in pharmacology · 2014Review
- While systolic cardiomyocyte function is preserved, diastolic myocyte function and recovery from acidosis are impaired in CaMKIIδ-KO mice.Journal of molecular and cellular cardiology · 2013Article
- Stretch current-induced abnormal impulses in CaMKIIδ knockout mouse ventricular myocytes.Journal of cardiovascular electrophysiology · 2013Article
- Regulation of vascular smooth muscle mechanotransduction by microRNAs and L-type calcium channels.Communicative & integrative biology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
rationaleRecent studies have highlighted important roles of CaMKII in regulating Ca(2+) handling and excitation-contraction coupling. However, the cardiac effect of chronic CaMKII inhibition has not been well understood.
objectiveWe have tested the alterations of L-type calcium current (I(Ca)) and cardiac function in CaMKIIdelta knockout (KO) mouse left ventricle (LV). METHODS AND
resultsWe used the patch-clamp method to record I(Ca) in ventricular myocytes and found that in KO LV, basal I(Ca) was significantly increased without changing the transmural gradient of I(Ca) distribution. Substitution of Ba(2+) for Ca(2+) showed similar increase in I(Ba). There was no change in the voltage dependence of I(Ca) activation and inactivation. I(Ca) recovery from inactivation, however, was significantly slowed. In KO LV, the Ca(2+)-dependent I(Ca) facilitation (CDF) and I(Ca) response to isoproterenol (ISO) were significantly reduced. However, ISO response was reversed by beta2-adrenergic receptor (AR) inhibition. Western blots showed a decrease in beta1-AR and an increase in Ca(v)1.2, beta2-AR, and Galphai3 protein levels. Ca(2+) transient and sarcomere shortening in KO myocytes were unchanged at 1-Hz but reduced at 3-Hz stimulation. Echocardiography in conscious mice revealed an increased basal contractility in KO mice. However, cardiac reserve to work load and beta-adrenergic stimulation was reduced. Surprisingly, KO mice showed a reduced heart rate in response to work load or beta-adrenergic stimulation.
conclusionsOur results implicate physiological CaMKII activity in maintaining normal I(Ca), Ca(2+) handling, excitation-contraction coupling, and the in vivo heart function in response to cardiac stress.
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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.