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EARLY-STAGE ATHEROSCLEROSIS begins when 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 called 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 atherosclerotic deposits. This process can be stopped if an antioxidant, such as AGI-1067, blocks the oxidant signal (inset).
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Image: ALICE Y. CHEN
In the early 1990s the root causes of atherosclerosis had started to become clearer. Emerging research showed that the disease bore a direct relation to inflammation triggered by lipoproteins and other agents that spurred growth of atherosclerotic deposits.
Taking note of these discoveries, clinical researchers had begun to mull how they could intervene to block this process. Two professors at the Emory University School of Medicine--Russell M. Medford and R. Wayne Alexander, both cardiologists and biologists--were intrigued by findings that tied inflammation to oxidants, molecules that strip electrons from other molecules.
This article was originally published with the title Signal Jammer.
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