Key result
Cyclic stretch via stress fibers modulates nuclear mechanics to drive vascular remodeling in hypertension.
Why the study?
The cellular mechanisms initiating and terminating aortic wall thickening as a smooth muscle adaptation during hypertension remain unclear.
Stress fibers in vascular smooth muscle cells act as mechanosensors that modulate nuclear mechanics during hypertensive arterial wall thickening.
Should not yet change clinical hypertension management; extends mechanistic insights into vascular remodeling.
Aortic wall thickening under hypertension is regarded as a smooth muscle adaptation to restore homeostasis. However, the cellular mechanisms initiating and terminating this response remain unclear. Hypertension induces mechanical stimuli—such as hydrostatic pressure, interstitial shear stress, and cyclic stretch—that may trigger cellular adaptation. We hypothesized that cyclic stretch transmitted via stress fibers regulates both the onset and cessation of this process. To test this, we quantified strain along stress fiber orientation under hypertensive and adaptive conditions. Our results suggest that stress fibers modulate nuclear mechanics and act as mechanosensors in vascular remodeling during hypertension.
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Shukei Sugita (2026) studied Hypertension. Cyclic stretch was evaluated on Strain along stress fiber orientation. Cyclic stretch transmitted via stress fibers modulates nuclear mechanics and acts as a mechanosensor in vascular remodeling during hypertension.
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