Fig. 5

Conceptual model: In the carotid bifurcation, a common area for atherosclerosis development, disturbed flow causes GCX-mediated impairment of caveolae expression and eNOS-associated function. Specifically, in DF conditions GCX is diminished and, in turn, causes caveolae to be scarce and to exhibit diffuse localization, reduces eNOS-pS1177 expression, and disrupts caveolae and eNOS-pS1177 colocalization. These events are likely to weaken NO signaling and increase the risk of endothelial-dependent atherosclerosis. In UF conditions GCX is healthy and intact. As a result, caveolae is abundant and exhibits localization that is polarized to the subcellular region upstream of the flow direction. This expression and distribution of the caveolae coincides with elevated eNOS-pS1177 expression and colocalization with eNOS-pS1177, which is necessary for anti-atherosclerotic NO signaling