Key result
Mathematical modeling revealed that mechanical coupling and mechano-electrical feedback between cardiomyocytes and fibroblasts significantly depolarize resting potentials and increase susceptibility to triggered arrhythmias during calcium overload.
Why the study?
Fibroblast-cardiomyocyte electromechanical interactions noticeably affect myocardial electrical and mechanical function, but the mechanisms of spontaneous activity during calcium overload remain incompletely understood.
In silico modeling demonstrates that mechanical coupling and mechano-electrical feedback between fibroblasts and cardiomyocytes significantly increase susceptibility to arrhythmias during calcium overload.
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Hypothesis-generating for fibroblast-driven spontaneous activity in fibrosis; clinical relevance requires prospective validation.
Kursanov et al. (2023) studied Arrhythmia. Cardiomyocyte-fibroblast electromechanical interaction vs. Electrical interaction only or isolated cardiomyocyte was evaluated on Resting membrane potential depolarization and triggered activity (EADs and extrasystoles). Mathematical modeling revealed that mechanical coupling and mechano-electrical feedback between cardiomyocytes and fibroblasts significantly depolarize resting potentials and increase susceptibility to triggered arrhythmias during calcium overload.
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