ReviewThe Journal of clinical investigation2006
Dichotomy of Ca2+ in the heart: contraction versus intracellular signaling.
Review in The Journal of clinical investigation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed, 100 citations in OpenAlex.
- Cardiac Localized Polycystin-2 in the Natriuretic Peptide Signaling Pathway and Hypertension.Journal of the American Society of Nephrology : JASN · 2025Article
- Design and Applications of Genetically-Encoded Voltage-Dependent Calcium Channel Inhibitors.Handbook of experimental pharmacology · 2023Review
- Inositol 1,4,5-trisphosphate receptors in cardiomyocyte physiology and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Store-Operated Calcium Entry in the Cardiovascular System.Advances in experimental medicine and biology · 2021Review
- The First Heartbeat-Origin of Cardiac Contractile Activity.Cold Spring Harbor perspectives in biology · 2020Review
- Alteration of calcium signalling in cardiomyocyte induced by simulated microgravity and hypergravity.Cell proliferation · 2020Article
- Blockade of L-type CaScientific reports · 2019Article
- Engineering selectivity into RGK GTPase inhibition of voltage-dependent calcium channels.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Endothelin-1 promotes hypertrophic remodelling of cardiac myocytes by activating sustained signalling and transcription downstream of endothelin type A receptors.Cellular signalling · 2017Article
- Vitamin D, reactive oxygen species and calcium signalling in ageing and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Review
- Cardiac Stim1 Silencing Impairs Adaptive Hypertrophy and Promotes Heart Failure Through Inactivation of mTORC2/Akt Signaling.Circulation · 2016Article
- Article
- The type 2 inositol 1,4,5-trisphosphate receptor, emerging functions for an intriguing Ca²⁺-release channel.Biochimica et biophysica acta · 2015Review
- TRPC3 contributes to regulation of cardiac contractility and arrhythmogenesis by dynamic interaction with NCX1.Cardiovascular research · 2015Article
- Succinate causes pathological cardiomyocyte hypertrophy through GPR91 activation.Cell communication and signaling : CCS · 2014Article
- Differential effects of hypoxic and hyperoxic stress-induced hypertrophy in cultured chick fetal cardiac myocytes.In vitro cellular & developmental biology. Animal · 2014Article
- Effects of wenxin keli on the action potential and L-type calcium current in rats with transverse aortic constriction-induced heart failure.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- STIM1-dependent store-operated Ca²⁺ entry is required for pathological cardiac hypertrophy.Journal of molecular and cellular cardiology · 2012Article
- Plasma membrane calcium pump (PMCA4)-neuronal nitric-oxide synthase complex regulates cardiac contractility through modulation of a compartmentalized cyclic nucleotide microdomain.The Journal of biological chemistry · 2011Article
- Calcium signaling in cardiac myocytes.Cold Spring Harbor perspectives in biology · 2011Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca2+ plays a pivotal role in both excitation-contraction coupling (ECC) and activation of Ca2+-dependent signaling pathways. One of the remaining questions in cardiac biology is how Ca2+-dependent signaling pathways are regulated under conditions of continual Ca2+ transients that mediate cardiac contraction during each heartbeat. Ca2+-calmodulin-dependent protein kinase II (CaMKII) activation and its ability to regulate histone deacetylase 5 (HDAC5) nuclear shuttling represent a critical Ca2+-dependent signaling circuit for controlling cardiac hypertrophy and heart failure, yet the mechanism of activation by Ca2+ is not known. In this issue of the JCI, Wu et al. convincingly demonstrate that the inositol 1,4,5-trisphosphate receptor (InsP3R) is involved in local control of Ca2+ for activating CaMKII in the nuclear envelope of adult ventricular cardiac myocytes (see the related article beginning on page 675). The overall paradigm that is demonstrated is the best example of a molecular mechanism whereby signaling is directly regulated by a local Ca2+ pool that is disparate or geometrically insensitive to cytosolic Ca2+ underlying each contractile cycle.
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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.