Key result
Mechano-electric feedback extends cardiomyocyte spatial correlation length ~10-fold, enabling near system-wide synchronization.
Why the study?
Standard dipole models predict only short-range phase coherence due to the 1/r^3 decay of elastic interactions, leaving tissue-scale mechanical coordination of cardiomyocytes unexplained.
A computational model demonstrates that mechano-electric feedback enables long-range mechanical synchronization of cardiomyocytes, offering insights into cardiac tissue engineering and arrhythmogenesis.
Challenges short-range dipole predictions for cardiomyocyte coherence; leaves open whether mechano-electric feedback enables tissue-scale synchronization in vivo.
Long-range synchronization of cardiomyocytes via purely elastic substrates is limited by the 1/r^3 decay of mechanical interactions. Standard dipole models therefore predict only short-range phase coherence, leaving tissue-scale coordination unexplained. In this work, I introduce a state-dependent network model in which local phase coherence enhances contractile force through mechano-electric feedback. Numerical simulations on a 1D chain show that this feedback extends the spatial correlation length by about an order of magnitude (from ξ ≈ 1.2 to ξ ≳ 20 cell spacings), enabling near system-wide synchronization within the simulated system sizes. I further identify a transition boundary in the stiffness-feedback plane and show that cellular alignment reduces the critical feedback strength by a factor of two to three. These results provide a mechanical basis for the roles of substrate compliance and orientational order in cardiac tissue engineering, and suggest a possible physical pathway for arrhythmogenesis in fibrotic tissue.
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Hiroyuki Morimura (2026) studied this question. Mechano-electric feedback in cardiomyocytes extends spatial correlation length by an order of magnitude (from ~1.2 to >20 cell spacings), enabling near system-wide synchronization.
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