ArticleBiophysical journal2007
Kinetic properties of the cardiac L-type Ca2+ channel and its role in myocyte electrophysiology: a theoretical investigation.
Article in Biophysical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 131 citations in OpenAlex.
- Mechanisms of cardiomyocyte dysfunction induced by extracellular histones.Cell death discovery · 2026Article
- A novel computational model of swine ventricular myocyte reveals new insights into disease mechanisms and therapeutic approaches in Timothy Syndrome.Scientific reports · 2024Article
- Transmural APD heterogeneity determines ventricular arrhythmogenesis in LQT8 syndrome: Insights from Bidomain computational modeling.PloS one · 2024Article
- Local Control Model of a Human Ventricular Myocyte: An Exploration of Frequency-Dependent Changes and Calcium Sparks.Biomolecules · 2023Article
- CACNA1C-Related Channelopathies.Handbook of experimental pharmacology · 2023Review
- Models of the cardiac L-type calcium current: A quantitative review.WIREs mechanisms of disease · 2023Review
- Exploring the Coordination of Cardiac Ion Channels With Action Potential Clamp Technique.Frontiers in physiology · 2022Review
- Shexiang Baoxin Pills Could Alleviate Isoproterenol-Induced Heart Failure Probably through its Inhibition of CaV1.2 Calcium Channel Currents.Biochemistry research international · 2022Article
- Calcium-dependent inactivation controls cardiac L-type CaThe Journal of general physiology · 2019Article
- Cardiovascular disease models: A game changing paradigm in drug discovery and screening.Biomaterials · 2019Review
- A Mathematical Model of the Human Cardiac NaThe Journal of membrane biology · 2019Article
- Computational models in cardiology.Nature reviews. Cardiology · 2019Review
- A bilobal model of CaThe Journal of general physiology · 2018Article
- Micro- and nano-patterned conductive graphene-PEG hybrid scaffolds for cardiac tissue engineering.Chemical communications (Cambridge, England) · 2017Article
- Studying dyadic structure-function relationships: a review of current modeling approaches and new insights into CaClinical Medicine Insights. Cardiology · 2017Article
- Computational Cardiac Modeling Reveals Mechanisms of Ventricular Arrhythmogenesis in Long QT Syndrome Type 8:Frontiers in physiology · 2017Article
- Species-Dependent Mechanisms of Cardiac Arrhythmia: A Cellular Focus.Clinical Medicine Insights. Cardiology · 2017Review
- Pro-arrhythmogenic effects of CACNA1C G1911R mutation in human ventricular tachycardia: insights from cardiac multi-scale models.Scientific reports · 2016Article
- Reconstruction of Cell Surface Densities of Ion Pumps, Exchangers, and Channels from mRNA Expression, Conductance Kinetics, Whole-Cell Calcium, and Current-Clamp Voltage Recordings, with an Application to Human Uterine Smooth Muscle Cells.PLoS computational biology · 2016Article
- Mechanisms of astrocytic K(+) clearance and swelling under high extracellular K(+) concentrations.The journal of physiological sciences : JPS · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The L-type Ca(2+) channel (Ca(V)1.2) plays an important role in action potential (AP) generation, morphology, and duration (APD) and is the primary source of triggering Ca(2+) for the initiation of Ca(2+)-induced Ca(2+)-release in cardiac myocytes. In this article we present: 1), a detailed kinetic model of Ca(V)1.2, which is incorporated into a model of the ventricular mycoyte where it interacts with a kinetic model of the ryanodine receptor in a restricted subcellular space; 2), evaluation of the contribution of voltage-dependent inactivation (VDI) and Ca(2+)-dependent inactivation (CDI) to total inactivation of Ca(V)1.2; and 3), description of dynamic Ca(V)1.2 and ryanodine receptor channel-state occupancy during the AP. Results are: 1), the Ca(V)1.2 model reproduces experimental single-channel and macroscopic-current data; 2), the model reproduces rate dependence of APD, [Na(+)](i), and the Ca(2+)-transient (CaT), and restitution of APD and CaT during premature stimuli; 3), CDI of Ca(V)1.2 is sensitive to Ca(2+) that enters the subspace through the channel and from SR release. The relative contributions of these Ca(2+) sources to total CDI during the AP vary with time after depolarization, switching from early SR dominance to late Ca(V)1.2 dominance. 4), The relative contribution of CDI to total inactivation of Ca(V)1.2 is greater at negative potentials, when VDI is weak; and 5), loss of VDI due to the Ca(V)1.2 mutation G406R (linked to the Timothy syndrome) results in APD prolongation and increased CaT.
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Registered trials
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