ArticleScientific reports2026
A novel computational model of human iPSC-derived ventricular myocytes with improved L-type calcium current for application to Timothy syndrome.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are a powerful platform for modeling inherited arrhythmias, yet current in silico representations face limitations in Ca2+ handling. Here, we present a novel ventricular hiPSC-CM ionic model incorporating a Markovian formulation of the L-type Ca2+ current (I[Formula: see text]), tailored to better recapitulate Ca[Formula: see text] dynamics and voltage-dependent inactivation. The model was calibrated against experimental data from hiPSC-CMs derived from a healthy individual and validated through a series of simulations relevant to both physiological and pathological conditions. These included pharmacological inhibition of I[Formula: see text] with nifedipine, Ca[Formula: see text] overload and DAD-mediated triggered activity, and the interplay between intracellular Ca[Formula: see text] cycling and membrane mechanisms in driving automaticity. Sensitivity analysis was used to generate a population of models capturing intercellular variability. In addition, the model was able to reproduce the effects of genetic mutations in the L-type Ca[Formula: see text] channel, including those associated with Timothy Syndrome, providing an additional layer of validation. Overall, this computational framework offers a flexible and physiologically grounded tool for investigating the mechanisms of arrhythmogenesis in hiPSC-CMs and for supporting personalized medicine applications.
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