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. Author manuscript; available in PMC: 2015 Jun 24.
Published in final edited form as: Circulation. 2014 May 7;129(25):2629–2632. doi: 10.1161/CIRCULATIONAHA.114.010609

Figure 1.

Figure 1

Molecular mechanisms in the vascular wall leading to aortic dissection. In the presence of angiotensin II, endothelial Nox2-derived oxidants (·O2− and ONOO−) stimulate endothelial cyclophillin A (cypA) production, which acts as a paracrine factor to activate metalloproteinases (MMPs) and ROS production in VSMC. MMPs, in turn, degrade elastin, causing aortic dissection. Angiotensin II elicits an array of oxidants (·O−2, ONOO−, H2O2) and inflammatory responses (NFκβ) within the arterial wall via AT1 receptors (AT1R), which stimulate VSMC and fibroblast proliferation and inflammatory influx in the vascular wall, all contributing to remodeling and fibrosis. Angiotensin II also stimulates cypA production in VSMC, further contributing to oxidants and inflammation.