ReviewCold Spring Harbor perspectives in biology2011
Calcium signaling in cardiac myocytes.
Review in Cold Spring Harbor perspectives in biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 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.
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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
140 citing papers in PubMed, 333 citations in OpenAlex.
- Evaluating the Whole Blood Survival Advantage: How Citrate and Calcium Levels Drive Mortality in a Translational Swine Model of Polytrauma.Journal of the American College of Emergency Physicians open · 2026Article
- Polydopamine Nanotubes: Multifunctional Smart Nanotransducers for Cellular Activity Modulation.ACS nano · 2026Article
- Sequential changes in calcium transients during M phase regulate cardiomyocyte proliferation.The Journal of cell biology · 2026Article
- Fluorescence Lifetime Spectroscopy Reveals Distinct Allosteric Mechanisms of SERCA Inhibitors.The Journal of membrane biology · 2026Article
- Fatty Acids and Their Roles in Cardiac Physiology and Pathology: Mechanistic and Interventional Studies.Nutrients · 2026Review
- Investigating PKD2 deficiency-associated cardiomyopathies using hESC-cardiomyocytes and bioengineered 3D ventricular cardiac tissue strips.Cell death & disease · 2026Article
- Multi-omic analyses identify molecular targets of Chd7 that contribute to CHARGE syndrome model phenotypes.Disease models & mechanisms · 2026Article
- Integrated bioinformatic and in vivo analysis confirms the cardioprotective role of OPA1.BMC cardiovascular disorders · 2025Article
- Modulating the Expression of Exercise-induced lncRNAs: Implications for Cardiovascular Disease Progression.Journal of cardiovascular translational research · 2025Review
- Cardiomyocyte maturation and proliferation is a flip coin.BMC cardiovascular disorders · 2025Review
- Calcium signalling and organelle crosstalk in cardiovascular disease: an interplay of cardiac cell death pathways.Molecular biology reports · 2025Review
- Copper Chelation by Penicillamine Protects Against Doxorubicin-Induced Cardiomyopathy by Suppressing FDX1-Mediated Cuproptosis.Biomolecules · 2025Article
- Healthy human induced pluripotent stem cell-derived cardiomyocytes exhibit sex dimorphism even without the addition of hormones.Stem cells (Dayton, Ohio) · 2025Article
- Vitamin C as a Cardioprotective Agent Against Doxorubicin-Induced Cardiotoxicity.Journal of the American Heart Association · 2025Review
- Valproate independently activates Snf1, inhibits TORC1, and induces repression of INO1 transcription by increasing nuclear localization of Opi1.Scientific reports · 2025Article
- SERCA2a dysfunction in the pathophysiology of heart failure with preserved ejection fraction: a direct role is yet to be established.Heart failure reviews · 2025Review
- Longevity mechanisms in cardiac aging: exploring calcium dysregulation and senescence.Biogerontology · 2025Review
- A CaJournal of mathematical biology · 2025Article
- PGRMC2 is a pressure-volume regulator critical for myocardial responses to stress in mice.Nature communications · 2025Article
- Mitochondrial calcium uniporter complex: An emerging therapeutic target for cardiovascular diseases (Review).International journal of molecular medicine · 2025Review
80 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Calcium (Ca(2+)) is a critical regulator of cardiac myocyte function. Principally, Ca(2+) is the link between the electrical signals that pervade the heart and contraction of the myocytes to propel blood. In addition, Ca(2+) controls numerous other myocyte activities, including gene transcription. Cardiac Ca(2+) signaling essentially relies on a few critical molecular players--ryanodine receptors, voltage-operated Ca(2+) channels, and Ca(2+) pumps/transporters. These moieties are responsible for generating Ca(2+) signals upon cellular depolarization, recovery of Ca(2+) signals following cellular contraction, and setting basal conditions. Whereas these are the central players underlying cardiac Ca(2+) fluxes, networks of signaling mechanisms and accessory proteins impart complex regulation on cardiac Ca(2+) signals. Subtle changes in components of the cardiac Ca(2+) signaling machinery, albeit through mutation, disease, or chronic alteration of hemodynamic demand, can have profound consequences for the function and phenotype of myocytes. Here, we discuss mechanisms underlying Ca(2+) signaling in ventricular and atrial myocytes. In particular, we describe the roles and regulation of key participants involved in Ca(2+) signal generation and reversal.
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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.