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Computational analysis of the role of mechanosensitive Notch signaling in arterial adaptation to hypertension. | LitMetric

Computational analysis of the role of mechanosensitive Notch signaling in arterial adaptation to hypertension.

J Mech Behav Biomed Mater

Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, the Netherlands; Institute for Complex Molecular Systems, Eindhoven University of Technology, Eindhoven, the Netherlands. Electronic address:

Published: September 2022

AI Article Synopsis

  • Arteries adapt and change their structure in response to mechanical forces, with hypertension causing thickening of the arterial walls.
  • The role of Notch signaling between vascular smooth muscle cells (VSMCs) in this process was investigated through a computational model that combined arterial mechanics and Notch signaling.
  • The study found that Notch's sensitivity to blood pressure strain may significantly influence arterial thickening in hypertension, suggesting that targeting Notch mechanisms could be a strategy for managing vascular changes related to high blood pressure.

Article Abstract

Arteries grow and remodel in response to mechanical stimuli. Hypertension, for example, results in arterial wall thickening. Cell-cell Notch signaling between vascular smooth muscle cells (VSMCs) is known to be involved in this process, but the underlying mechanisms are still unclear. Here, we investigated whether Notch mechanosensitivity to strain may regulate arterial thickening in hypertension. We developed a multiscale computational framework by coupling a finite element model of arterial mechanics, including residual stress, to an agent-based model of mechanosensitive Notch signaling, to predict VSMC phenotypes as an indicator of growth and remodeling. Our simulations revealed that the sensitivity of Notch to strain at mean blood pressure may be a key mediator of arterial thickening in hypertensive arteries. Further simulations showed that loss of residual stress can have synergistic effects with hypertension, and that changes in the expression of Notch receptors, but not Jagged ligands, may be used to control arterial growth and remodeling and to intensify or counteract hypertensive thickening. Overall, we identify Notch mechanosensitivity as a potential mediator of vascular adaptation, and we present a computational framework that can facilitate the testing of new therapeutic and regenerative strategies.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7613661PMC
http://dx.doi.org/10.1016/j.jmbbm.2022.105325DOI Listing

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