Biomechanical factors as triggers of vascular growth

Abstract

Haemodynamic factors influence all forms of vascular growth (vasculogenesis, angiogenesis, arteriogenesis). Because of its prominent role in atherosclerosis, shear stress has gained particular attention, but other factors such as circumferential stretch are equally important to maintain the integrity and to (re)model the vascular network. While these haemodynamic forces are crucial determinants of the appearance and the structure of the vasculature, they are in turn subjected to structural changes in the blood vessels, such as an increased arterial stiffness in chronic arterial hypertension and ageing. This results in an interplay between the various forces (biomechanical forces) and the involved vascular elements. Although many molecular mediators of biomechanical forces still need to be identified, there is plenty of evidence for the causal role of these forces in vascular growth processes, which will be summarized in this review. In addition, we will discuss the effects of concomitant diseases and disorders on these processes by altering either the biomechanics or their transduction into biological signals. Particularly endothelial dysfunction, diabetes, hypercholesterolaemia, and age affect mechanosensing and -transduction of flow signals, thereby underpinning their influence on cardiovascular health. Finally, current approaches to modify biomechanical forces to therapeutically modulate vascular growth in humans will be described.

Mechanical Stresses, Arterial Stiffness, and Brain Small Vessel Diseases

“…12,13 SS is increased by elevation of blood flow and blood viscosity, but decreased by arterial dilatation. 12 In general, high SS causes vessel dilatation and atheroprotection through endothelial stimulation. In the chronic phase, an alteration in mechanical stresses causes arterial remodeling.…”

“…12 In association with an elevation of PWV, blood flow and BP increase during systole and decrease during diastole. Because higher WT and lower SS are assumed to be atherogenic, [12][13][14][15][16][17] peak systolic WT and end-diastolic SS may underlie the association between baPWV and atherosclerosis. In fact, in the present study, simple correlation coefficients with baPWV were significantly higher for systolic WT (r=0.58 for SBP; r=0.55 for SBP2) than for diastolic WT (r=0.43; P<0.0001).…”

“…12,15 However, studies evaluating potential alterations of mechanical stresses related to arterial stiffness are limited.…”

“…12,13 Circumferential wall tension (WT) and longitudinal shear stress (SS) are major mechanical stresses and cause acute and chronic changes in arterial function and structure. [12][13][14][15] In the carotid artery, higher WT and lower SS are associated with carotid arterial remodeling. 16,17 WT was suggested to cause stretching of the arterial wall resulting in arterial hypertrophy, whereas reduced SS causes endothelial…”

Panta rhei: Everything flows - flow is everything Comment on Buschmann et al, p. 317 - 324

“…(E)ECP leads to continuous perfusion improvement by triggering adaptive vessel growth in response to the biomechanic alterations in the vasculature [7]. One of the fi rst researchers to recognise the mechanistic diff erences between angiogenesis, i.e.…”