Key result
The integration of stretch-activated, Na+, and mechano-gated currents in computational models increased myocyte segment force by 13.8–36.6% and decreased element length by 12.1–31.5% in isosarcometric contraction.
Why the study?
Although electrophysiological mechanisms are largely known, the roles of stretch-activated currents and myofibroblast currents in cardiac mechanics remain debated.
Population
Integrated mathematical model of human atrial myocyte and myofibroblast
Comparison
Changes in basic cycle length, number of coupled Mfbs, and intercellular coupling conductance
Design
Mathematical modeling study
Authors
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Supports SAC/MGC targeting for AF conversion; extends Mfb contributions beyond myocytes in arrhythmia models.
Stretch-activated currents in myocytes and Na+/mechano-gated currents in myofibroblasts significantly regulate myocyte mechanical behavior in computational models.
Zhan et al. (2019) studied Atrial fibrillation and cardiac fibrosis (computational model). Integration of stretch-activated current (ISAC), Na+ current (INa_Mfb), and mechano-gated channels' current (IMGC_Mfb) vs. Myocyte models without myofibroblast coupling or without these specific currents was evaluated on Myocyte mechanical parameters (segment force and element length). The integration of stretch-activated, Na+, and mechano-gated currents in computational models increased myocyte segment force by 13.8–36.6% and decreased element length by 12.1–31.5% in isosarcometric contraction.
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