ArticleBiophysical journal2007
Modeling hypertrophic IP3 transients in the cardiac myocyte.
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 21 papers.
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Who cites it
21 citing papers in PubMed, 57 citations in OpenAlex.
- Sodium-myo-inositol cotransporter-1, SMIT1, promotes cardiac hypertrophy and fibrosis induced by pressure overload in mice.Cardiovascular research · 2026Article
- Modeling the interplay of sex hormones in cardiac hypertrophic signaling.PLoS computational biology · 2025Article
- Review
- Mechanisms underlying divergent relationships between CaThe Journal of physiology · 2023Article
- Systems modeling predicts that mitochondria ER contact sites regulate the postsynaptic energy landscape.NPJ systems biology and applications · 2021Article
- Involvement of Histamine 2 Receptor in Alpha 1 Adrenoceptor Mediated Cardiac Hypertrophy and Oxidative Stress in H9c2 Cardio Myoblasts.Journal of cardiovascular translational research · 2021Article
- CaBiophysical journal · 2020Article
- Three dimensional coupled reaction-diffusion modeling of calcium and inositol 1,4,5-trisphosphate dynamics in cardiomyocytes.RSC advances · 2019Article
- Mechanisms Underlying Spontaneous Action Potential Generation Induced by Catecholamine in Pulmonary Vein Cardiomyocytes: A Simulation Study.International journal of molecular sciences · 2019Article
- Mechanical regulation of gene expression in cardiac myocytes and fibroblasts.Nature reviews. Cardiology · 2019Review
- Quantitative systems models illuminate arrhythmia mechanisms in heart failure: Role of the NaWiley interdisciplinary reviews. Systems biology and medicine · 2019Review
- Modular modelling with Physiome standards.The Journal of physiology · 2016Article
- Mathematical modeling of cardiac growth and remodeling.Wiley interdisciplinary reviews. Systems biology and medicine · 2016Review
- Calcium and IP3 dynamics in cardiac myocytes: experimental and computational perspectives and approaches.Frontiers in pharmacology · 2014Review
- Network reconstruction and systems analysis of cardiac myocyte hypertrophy signaling.The Journal of biological chemistry · 2012Article
- Systems analysis of small signaling modules relevant to eight human diseases.Annals of biomedical engineering · 2011Article
- Computational models reduce complexity and accelerate insight into cardiac signaling networks.Circulation research · 2011Review
- Cardiac models in drug discovery and development: a review.Critical reviews in biomedical engineering · 2011Review
- CellML metadata standards, associated tools and repositories.Philosophical transactions. Series A, Mathematical, physical, and engineering sciences · 2009Article
- Sensitivity of NFAT cycling to cytosolic calcium concentration: implications for hypertrophic signals in cardiac myocytes.Biophysical journal · 2009Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy is a known risk factor for heart disease, and at the cellular level is caused by a complex interaction of signal transduction pathways. The IP3-calcineurin pathway plays an important role in stimulating the transcription factor NFAT which binds to DNA cooperatively with other hypertrophic transcription factors. Using available kinetic data, we construct a mathematical model of the IP3 signal production system after stimulation by a hypertrophic alpha-adrenergic agonist (endothelin-1) in the mouse atrial cardiac myocyte. We use a global sensitivity analysis to identify key controlling parameters with respect to the resultant IP3 transient, including the phosphorylation of cell-membrane receptors, the ligand strength and binding kinetics to precoupled (with G(alpha)GDP) receptor, and the kinetics associated with precoupling the receptors. We show that the kinetics associated with the receptor system contribute to the behavior of the system to a great extent, with precoupled receptors driving the response to extracellular ligand. Finally, by reparameterizing for a second hypertrophic alpha-adrenergic agonist, angiotensin-II, we show that differences in key receptor kinetic and membrane density parameters are sufficient to explain different observed IP3 transients in essentially the same pathway.
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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.