ArticleBiophysical journal2014
Systems modeling of Ca(2+) homeostasis and mobilization in platelets mediated by IP3 and store-operated Ca(2+) entry.
Article in Biophysical journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Interplay between store-operated calcium entry and mitochondrial phosphate handling modulates force and fatigue during exercise.The Journal of physiology · 2026Article
- Platelet mitochondria dysfunction in diabetes mellitus: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Toll-like Receptor 7 Deficiency Attenuates Platelet Dysfunction in Sepsis.Biomolecules · 2025Article
- Molecular mechanism for platelet hyperreactivity in diabetes mellitus.Journal of diabetes investigation · 2025Article
- SEC61B regulates calcium flux and platelet hyperreactivity in diabetes.The Journal of clinical investigation · 2025Article
- Extended Modelling of Molecular Calcium Signalling in Platelets by Combined Recurrent Neural Network and Partial Least Squares Analyses.International journal of molecular sciences · 2025Article
- Platelets and diseases: signal transduction and advances in targeted therapy.Signal transduction and targeted therapy · 2025Review
- Platelets and mitochondria: the calcium connection.Molecular biology reports · 2025Review
- A review of natural compounds to regulate platelet aggregation: molecular mechanism and research advance.Frontiers in pharmacology · 2025Review
- Basal State Calibration of a Chemical Reaction Network Model for Autophagy.International journal of molecular sciences · 2024Article
- A Review of Quantitative Systems Pharmacology Models of the Coagulation Cascade: Opportunities for Improved Usability.Pharmaceutics · 2023Review
- Mechanisms underlying divergent relationships between CaThe Journal of physiology · 2023Article
- Optical uncaging of ADP reveals the early calcium dynamics in single, freely moving platelets.Biomedical optics express · 2020Article
- An Introductory Overview of Image-Based Computational Modeling in Personalized Cardiovascular Medicine.Frontiers in bioengineering and biotechnology · 2020Review
- In vivo measurement of blood clot mechanics from computational fluid dynamics based on intravital microscopy images.Computers in biology and medicine · 2019Article
- Cyclic nucleotide-dependent inhibitory signaling interweaves with activating pathways to determine platelet responses.Research and practice in thrombosis and haemostasis · 2018Review
- Method for the simulation of blood platelet shape and its evolution during activation.PLoS computational biology · 2018Article
- VEGFR1 promotes cell migration and proliferation through PLCγ and PI3K pathways.NPJ systems biology and applications · 2018Article
- Bile Acids Do Not Contribute to the Altered Calcium Homeostasis of Platelets from Rats with Biliary Cirrhosis.Frontiers in physiology · 2017Article
- Platelet signaling: a complex interplay between inhibitory and activatory networks.Journal of thrombosis and haemostasis : JTH · 2016Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Resting platelets maintain a stable level of low cytoplasmic calcium ([Ca(2+)]cyt) and high dense tubular system calcium ([Ca(2+)]dts). During thrombosis, activators cause a transient rise in inositol trisphosphate (IP3) to trigger calcium mobilization from stores and elevation of [Ca(2+)]cyt. Another major source of [Ca(2+)]cyt elevation is store-operated calcium entry (SOCE) through plasmalemmal calcium channels that open in response to store depletion as [Ca(2+)]dts drops. A 34-species systems model employed kinetics describing IP3-receptor, DTS-plasmalemma puncta formation, SOCE via assembly of STIM1 and Orai1, and the plasmalemma and sarco/endoplasmic reticulum Ca(2+)-ATPases. Four constraints were imposed: calcium homeostasis before activation; stable in zero extracellular calcium; IP3-activatable; and functional SOCE. Using a Monte Carlo method to sample three unknown parameters and nine initial concentrations in a 12-dimensional space near measured or expected values, we found that model configurations that were responsive to stimuli and demonstrated significant SOCE required high inner membrane electric potential (>-70 mV) and low resting IP3 concentrations. The absence of puncta in resting cells was required to prevent spontaneous store depletion in calcium-free media. Ten-fold increases in IP3 caused saturated calcium mobilization. This systems model represents a critical step in being able to predict platelets' phenotypes during hemostasis or thrombosis.
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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.