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Published October 2015 | Accepted Version
Journal Article Open

Blood flow modulation of vascular dynamics


Purpose of review: Blood flow is intimately linked with cardiovascular development, repair and dysfunction. The current review will build on the fluid mechanical principle underlying haemodynamic shear forces, mechanotransduction and metabolic effects. Recent findings: Pulsatile flow produces both time (∂τ/∂t) and spatial-varying shear stress (∂τ/∂x) to modulate vascular oxidative stress and inflammatory response with pathophysiological significance to atherosclerosis. The characteristics of haemodynamic shear forces, namely, steady laminar (∂τ/∂t = 0), pulsatile shear stress (PSS: unidirectional forward flow) and oscillatory shear stress (bidirectional with a near net 0 forward flow), modulate mechano-signal transduction to influence metabolic effects on vascular endothelial function. Atheroprotective PSS promotes antioxidant, anti-inflammatory and antithrombotic responses, whereas atherogenic oscillatory shear stress induces nicotinamide adenine dinucleotide phosphate oxidase–JNK signalling to increase mitochondrial superoxide production, protein degradation of manganese superoxide dismutase and post-translational protein modifications of LDL particles in the disturbed flow-exposed regions of vasculature. In the era of tissue regeneration, shear stress has been implicated in reactivation of developmental genes, namely, Wnt and Notch signalling, for vascular development and repair. Summary: Blood flow imparts a dynamic continuum from vascular development to repair. Augmentation of PSS confers atheroprotection and reactivation of developmental signalling pathways for regeneration.

Additional Information

© 2015 Wolters Kluwer Health, Inc. We would like to thank all members of Cardiovascular Engineering Research Laboratory for his assistance with the study. Funding: National Institutes of Health HL118650 (T.K.H.), HL083015 (T.K.H.), HL111437 (T.K.H.), T32HL007895 (R.R.S.P.), and AHA Pre-Doctoral Fellowship 15PRE21400019 (J.L.). Financial support and sponsorship: This work was supported by the NIH, AHA, and UCLA STAR program fellowship

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August 22, 2023
August 22, 2023