Key result
A morphomechanical model demonstrated that spontaneous embryonic heart c-looping can be modeled as a mechanical instability driven by residual stresses from tissue remodeling.
Why the study?
Before septation shapes the heart, the embryonic heart tube bends and twists during c-looping via cell remodeling, but the mechanical instability driving this torsional morphomechanics is incompletely characterized.
A morphomechanical model demonstrates that spontaneous embryonic heart looping can be modeled as a mechanical instability due to residual stresses from tissue remodeling.
Does not inform clinical practice; leaves open validation of residual stress mechanisms in congenital heart defects.
Before septation processes shape its four chambers, the embryonic heart is a straight tube that spontaneously bends and twists breaking the left-right symmetry. In particular, the heart tube is subjected to a cell remodeling inducing ventral bending and dextral torsion during the c-looping phase. In this work we propose a morphomechanical model for the torsion of the heart tube that behaves as a nonlinear elastic body. We hypothesize that this spontaneous looping can be modeled as a mechanical instability due to accumulation of residual stresses induced by the geometrical frustration of tissue remodeling, which mimics the cellular rearrangement within the heart tube. Thus, we perform a linear stability analysis of the resulting nonlinear elastic boundary value problem to determine the onset of c-looping as a function of the geometry of the tube and of the internal remodeling rate. We perform numerical simulations to study the fully nonlinear morphological transition, showing that the soft tube develops a realistic self-contacting looped shape in the physiological range of geometrical parameters.
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Bevilacqua et al. (2021) studied Embryonic heart c-looping. Morphomechanical modeling was evaluated on Onset of c-looping and morphological transition. A morphomechanical model demonstrated that spontaneous embryonic heart c-looping can be modeled as a mechanical instability driven by residual stresses from tissue remodeling.
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