atherogenesis

Atherogenesis is the process by which atheromatous plaques form in the walls of large- and medium-sized arteries, ultimately leading to atherosclerosis and cardiovascular disease. It initiates with endothelial dysfunction, increased permeability, and the adherence of circulating lipoproteins, particularly low-density lipoprotein (LDL), to the intima.

Low-density lipoproteins infiltrate the intima and become oxidized, triggering an inflammatory response. Monocytes adhere, migrate into the intima, and differentiate into macrophages that engulf oxidized LDL to become foam cells, forming fatty streaks. Smooth muscle cells migrate from the media into the intima, proliferate, and synthesize extracellular matrix, contributing to a growing fibrous cap. Over time, plaques may expand, calcify, or develop a necrotic lipid core; thinning of the fibrous cap and continued inflammation can produce plaque instability and rupture, which can precipitate thrombosis and acute vascular events.

Risk factors influence atherogenesis. Modifiable factors include hyperlipidemia, hypertension, diabetes mellitus, smoking, obesity, and physical inactivity. Non-modifiable factors include age, male sex, and family history. Genetic variations affecting lipoprotein metabolism, inflammation, or fibrinolysis can modify risk. Systemic inflammatory states and metabolic syndrome can accelerate the process.

Clinically, atherogenesis underlies coronary, carotid, cerebral, and peripheral arterial diseases. Detection relies on imaging methods such as carotid ultrasound, CT angiography, and MRI, as well as lipid and inflammatory biomarkers. Management emphasizes risk reduction and lipid lowering with statins, blood pressure control, antiplatelet therapy when appropriate, smoking cessation, and lifestyle modification. Research areas include anti-inflammatory strategies and therapies targeting lipoprotein handling and plaque stabilization.