Atherosclerosis is a focal disease that occurs predominantly at regions of the arterial tree that are exposed to disturbed blood flow, which generates low, oscillatory wall shear stress (WSS) at the lumen. WSS controls the spatial distribution of lesions by influencing numerous aspects of endothelial cell (EC) physiology, including inflammatory activation and viability. Of particular note, ECs in low shear, lesion-prone regions are characterized by increased apoptosis and turnover rates1 thus providing a potential explanation for the distinct spatial localization of lesion formation. Although the molecular mechanisms underlying the effects of WSS on EC physiology are poorly understood, they are known to involve transcriptional changes.

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