Atherosclerotic plaque

Atherosclerotic plaque is not a single molecule or receptor but rather a complex structure composed of fat, cholesterol, calcium deposits, inflammatory cells (such as macrophages), smooth muscle cells, extracellular matrix proteins (like fibronectin), and other blood-derived substances that accumulate within the walls of arteries. This buildup leads to thickening and stiffening of arterial walls—a process known as atherosclerosis—which narrows arteries and restricts blood flow. There are two main types: stable plaques that grow slowly and may eventually obstruct blood flow over time; and unstable (vulnerable) plaques that are prone to rupture even when not severely obstructive. Rupture can trigger clot formation (thrombosis), causing acute events such as heart attacks or strokes. The microenvironment within the plaque—including cell-cell interactions and matrix remodeling—plays a critical role in its progression or regression. While drugs like statins target lipid levels systemically rather than the plaque directly, some therapies such as anti-inflammatories (colchicine) or anticoagulants aim to stabilize existing plaques or prevent complications from rupture. However, \"atherosclerotic plaque\" itself is not considered a canonical molecular therapeutic target like an enzyme or receptor; instead it is the pathological manifestation resulting from multiple molecular processes.[1][2][5][6][9]

Other names

Arterial plaqueAtheromatous plaquePlaque (in context of atherosclerosis)

Anti-inflammatory action (e.g., colchicine inhibits microtubule formation and suppresses inflammation)[6]\nAnticoagulation to reduce thrombus formation on ruptured plaques[6]