Fig. 6: In the event of platelet activation, for example, by shear stress, sGC counterbalances proinflammatory activation of ECs, for example, by release of ANGPT1.

If sGC levels are reduced, for example, in the mouse model used in this study or in platelets of homozygous carriers of the CAD-associated risk variant, less ANGPT1 is released. Subsequently enhanced EC activation and leukocyte recruitment contribute to atherosclerotic plaque formation. This figure contains modified image material available at Servier Medical Art under a Creative Commons Attribution 3.0 Unported License.