Hemodynamics constitutes a critical factor in the formation of intracranial aneurysms. However, little is known about how an intracranial arterial wall responds to a hemodynamic insult, and how that response contributes to aneurysm formation. Unlike straight arterial segments (which respond to increased flow by expansive remodeling) and sinuses opposing bifurcation apices (which harbor recirculation flows and are prone to atherosclerotic development), aneurysmal degeneration occurs on the apical side of the bifurcation in the immediate peri-apical region, where flow creates very high wall shear stress (WSS) and wall shear stress gradient (WSSG)1. This results in destructive aneurysmal remodeling, characterized by loss of the internal elastic lamina (IEL) and thinning of the media. It is unknown how the unique hemodynamic conditions of combined high WSS and positive WSSG elicit these morphological changes, how the vascular wall responds to such insult at the molecular level, and what molecular mechanisms are involved.

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