Figure 7
From: High intraluminal pressure promotes vascular inflammation via caveolin-1
Mechanistic summary of pressure-induced inflammation. (1) Acute high intraluminal pressure exerts both low shear stress and circumferential stretch, (2) disassembling caveolae proteins (Cav1 and cavins) and causing flattening and reduction of caveolae. (3) This disassembly and/or pressure exertion leads to an increase in Nox-dependent ROS production, which in turn (4) results in an upregulation of arginase II activity and subsequently activating a feedback loop to further increase ROS production. (5) The increase in arginase II and ROS causes a translocation of NFkB into the nucleus resulting in increased gene and protein expression of adhesion molecules.
