Atherosclerosis

Atherosclerosis is not an individual molecule, protein, gene, or receptor. It is a chronic inflammatory disease process characterized by the buildup of plaques composed of fat, cholesterol, immune cells, calcium and other substances within arterial walls. This leads to narrowing and hardening of arteries and can result in reduced blood flow and increased risk for cardiovascular events such as heart attack and stroke. The underlying mechanisms involve complex interactions among lipids, inflammatory cells (like macrophages), endothelial dysfunction, smooth muscle cell proliferation/migration, extracellular matrix remodeling and thrombosis. While many molecular targets within this pathway have been identified—such as LDL receptors or inflammatory mediators like interleukin 1β—the term “atherosclerosis” refers specifically to the overall pathological process rather than any one therapeutic target. Because “atherosclerosis” describes an entire disease state/process rather than an individual druggable entity like an enzyme or receptor protein—and because it encompasses multiple pathways—it should not be listed as a canonical therapeutic target. In summary: Atherosclerosis is not considered an individual therapeutic target; it represents a complex pathological process involving many different cellular/molecular players. If you seek information about specific druggable targets relevant to this condition—such as LDL receptor (“Low-density lipoprotein receptor”), PCSK9 (“Proprotein convertase subtilisin/kexin type 9”), HMG-CoA reductase (“3-hydroxy-3-methylglutaryl-coenzyme A reductase”), CD31 (“Platelet endothelial cell adhesion molecule”)—please specify which one you need detailed information about.

Other names

Arteriosclerotic vascular disease (sometimes used interchangeably, but not strictly correct)Hardening of the arteries (lay term)