Early stage atherosclerosis begins whan an inflammatory agent attaches to an endothelial cell surface receptor (1). Resulting changes in the shape of the receptor generate an oxidant signal (2), which turns on a gene (3). The gene gives rise to a protein call vascular cell adhesion molecule-1 (VCAM-1) that migrates to the cell surface (4), where white blood cells attach to it (5), spurring events that lead to the buildup of atherosclerosis deposits.

This process can be stopped if an antioxidant, such as a designer drug (blue item in the insert), blocks the antioxidant signal.