ReviewAmerican journal of physiology. Heart and circulatory physiology2012
The interaction of Ca2+ with sarcomeric proteins: role in function and dysfunction of the heart.
Review in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 61 citations in OpenAlex.
- Effect of pimobendan on myocardial injury and systolic dysfunction in a canine model of supraventricular tachyarrhythmia.The Journal of veterinary medical science · 2025Article
- The Mechanism of Modulation of Cardiac Force by Temperature.International journal of molecular sciences · 2025Article
- An integrated picture of the structural pathways controlling the heart performance.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Contractile Behavior of Right Atrial Myocardium of Healthy Rats and Rats with the Experimental Model of Pulmonary Hypertension.International journal of molecular sciences · 2022Article
- Computationally efficient model of myocardial electromechanics for multiscale simulations.PloS one · 2021Article
- Phosphorylation of cardiac myosin-binding protein-C contributes to calcium homeostasis.The Journal of biological chemistry · 2020Article
- Cellular contractile forces are nonmechanosensitive.Science advances · 2020Article
- Mitochondrial mechanosensor in cardiovascular diseases.Vascular biology (Bristol, England) · 2020Review
- Myocardial Contractility: Historical and Contemporary Considerations.Frontiers in physiology · 2020Article
- Arrhythmogenic Current Generation by Myofilament-Triggered CaBiophysical journal · 2019Article
- Cardiotoxicity of environmental contaminant tributyltin involves myocyte oxidative stress and abnormal CaEnvironmental pollution (Barking, Essex : 1987) · 2019Article
- The lack of slow force response in failing rat myocardium: role of stretch-induced modulation of Ca-TnC kinetics.The journal of physiological sciences : JPS · 2019Article
- Inotropic interventions do not change the resting state of myosin motors during cardiac diastole.The Journal of general physiology · 2019Article
- Length-Dependent Activation of Contractility and Ca-Transient Kinetics in Auxotonically Contracting Isolated Rat Ventricular Cardiomyocytes.Frontiers in physiology · 2019Article
- The force and stiffness of myosin motors in the isometric twitch of a cardiac trabecula and the effect of the extracellular calcium concentration.The Journal of physiology · 2018Article
- Thick Filament Mechano-Sensing in Skeletal and Cardiac Muscles: A Common Mechanism Able to Adapt the Energetic Cost of the Contraction to the Task.Frontiers in physiology · 2018Article
- Article
- Myosin filament activation in the heart is tuned to the mechanical task.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Obesity alters molecular and functional cardiac responses to ischemia/reperfusion and glucagon-like peptide-1 receptor agonism.Basic research in cardiology · 2016Article
- Ablation of Matrix Metalloproteinase-9 Prevents Cardiomyocytes Contractile Dysfunction in Diabetics.Frontiers in physiology · 2016Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The hallmarks of the normal heartbeat are both rapid onset of contraction and rapid relaxation as well as an inotropic response to both increased end-diastolic volume and increased heart rate. At the microscopic level, Ca(2+) plays a crucial role in normal cardiac contraction. This paper reviews the cycle of Ca(2+) fluxes during the normal heartbeat, which underlie the coupling between excitation and contraction and permit a highly synchronized action of cardiac sarcomeres. Length dependence of the response of the regulatory sarcomeric proteins mediates the Frank-Starling Law of the heart. However, Ca(2+) transport may go astray in heart disease such as in congestive heart failure, and both jeopardize systole and diastole and triggering arrhythmias. The interaction between weak and strong segments in nonuniform cardiac muscle allows partial preservation of force of contraction but may further lead to mechanoelectric feedback or reverse excitation-contraction coupling mediating an early diastolic Ca(2+) transient caused by the rapid force decrease during the relaxation phase. These rapid force changes in nonuniform muscle may cause arrhythmogenic Ca(2+) waves to propagate by the activation of neighboring sarcoplasmic reticulum by diffusing Ca(2+) ions.
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What OpenQuestion holds
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.