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High wall shear stress and spatial gradients in vascular pathology: a review
Jennifer M Dolan1, John Kolega, Hui Meng
1Toshiba Stroke and Vascular Research Center, Clinical and Translational Research Center of the University at Buffalo, State University of New York, 875 Ellicott St., Buffalo, NY 14203, USA.
Insights
High wall shear stress (WSS) significantly impacts vascular health, promoting intracranial aneurysm (IA) formation and atherosclerotic plaque destabilization. Understanding endothelial cell responses to high WSS and WSS gradients is crucial for disease management.
Area of Science:
- Cardiovascular biology
- Biomedical engineering
- Pathology
Background:
- Cardiovascular diseases like intracranial aneurysms (IAs) and atherosclerosis often occur at sites of complex hemodynamics.
- Low wall shear stress (WSS) is linked to atherogenesis, but high WSS (>3 Pa) is increasingly recognized for its role in vascular biology and pathology.
Purpose of the Study:
- To review the role of high WSS in vascular pathologies.
- To elucidate endothelial cell (EC) responses to high WSS and WSS gradients (WSSG).
- To explore potential therapeutic targets for vascular diseases.
Main Methods:
- Review of existing literature on WSS, WSSG, and vascular remodeling.
- Analysis of EC mechanosensing mechanisms.
- Correlation of hemodynamic factors with pathological outcomes.
Main Results:
- Chronic high WSS promotes outward vascular remodeling, saccular IA formation, and atherosclerotic plaque destabilization.
- High WSS coupled with positive WSSG can initiate aneurysms.
- ECs are key sensors of WSS, mediating responses to hemodynamic forces.
Conclusions:
- High WSS is a critical factor in pathological vascular remodeling and disease initiation.
- Understanding EC responses to WSS and WSSG is vital for developing new treatments for IAs and atherosclerosis.
- Targeting EC mechanosensing pathways may offer novel therapeutic strategies.
Abstract:
Cardiovascular pathologies such as intracranial aneurysms (IAs) and atherosclerosis preferentially localize to bifurcations and curvatures where hemodynamics are complex. While extensive knowledge about low wall shear stress (WSS) has been generated in the past, due to its strong relevance to atherogenesis, high WSS (typically >3 Pa) has emerged as a key regulator of vascular biology and pathology as well, receiving renewed interests. As reviewed here, chronic high WSS not only stimulates adaptive outward remodeling, but also contributes to saccular IA formation (at bifurcation apices or outer curves) and atherosclerotic plaque destabilization (in stenosed vessels). Recent advances in understanding IA pathogenesis have shed new light on the role of high WSS in pathological vascular remodeling. In complex geometries, high WSS can couple with significant spatial WSS gradient (WSSG). A combination of high WSS and positive WSSG has been shown to trigger aneurysm initiation. Since endothelial cells (ECs) are sensors of WSS, we have begun to elucidate EC responses to high WSS alone and in combination with WSSG. Understanding such responses will provide insight into not only aneurysm formation, but also plaque destabilization and other vascular pathologies and potentially lead to improved strategies for disease management and novel targets for pharmacological intervention.
