Vascular smooth muscle cells (VSM) modulate cardiac output, maintain vascular pressure, and regulate blood flow via contraction. This contraction is generated by a mechanochemical interaction of actin-myosin cross-bridges within each cell and is governed by the biochemical and mechanical state of the cell [1]. When this state is disturbed, VSM cells can respond with excessive constriction (which can lead to hypertension) or weakened residual stresses (which can result in aortic aneurysms); both of which are considered to be symptoms of cardiovascular diseases [2]. Furthermore, disruption in the state of VSM cells can cause their migration into the intimal layer of the artery, which is a precursor to atherosclerosis.

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