Mechanical forces such as stretch and shear stress initiate complex signal transduction cascades and mechanotransduction via the cytoskeleton, leading to vascular remodeling.
This review highlights the molecular mechanisms by which vascular cells detect and respond to hemodynamic forces, leading to vascular remodeling.
Blood vessels are permanently subjected to mechanical forces in the form of stretch, encompassing cyclic mechanical strain due to the pulsatile nature of blood flow and shear stress. Significant variations in mechanical forces, of physiological or physiopathological nature, occur in vivo. These are accompanied by phenotypical modulation of smooth muscle cells and endothelial cells, producing structural modifications of the arterial wall. In all the cases, vascular remodelling can be allotted to a modification of the tensional strain or shear, and underlie a trend to reestablish baseline mechanical conditions. Vascular cells are equipped with numerous receptors that allow them to detect and respond to the mechanical forces generated by pressure and shear stress. The cytoskeleton and other structural components have an established role in mechanotransduction, being able to transmit and modulate tension within the cell via focal adhesion sites, integrins, cellular junctions and the extracellular matrix. Mechanical forces also initiate complex signal transduction cascades, including nuclear factor-kappaB and mitogen-activated protein kinase pathways, leading to functional changes within the cell.
Lehoux et al. (Thu,) conducted a review in Vascular responses to haemodynamic forces. Mechanical forces such as stretch and shear stress initiate complex signal transduction cascades and mechanotransduction via the cytoskeleton, leading to vascular remodeling.