Arterial inflammation

Arterial inflammation is a pathological immune response within the blood vessel walls, primarily driven by the accumulation of modified lipoproteins and mechanical stress. It involves the activation of the vascular endothelium, recruitment of monocytes and T-cells, and the subsequent formation of foam cells within the intima (Nature Reviews Cardiology, 2019). This chronic inflammatory state is the fundamental driver of atherosclerosis, leading to plaque progression, instability, and eventually rupture, which triggers clinical events such as myocardial infarction and stroke (The New England Journal of Medicine, 2017). While not a single molecular target, arterial inflammation represents a critical therapeutic focus; clinical trials like CANTOS and COLCOT have demonstrated that modulating inflammatory pathways, specifically the IL-1β/IL-6 axis, can significantly reduce cardiovascular risk independently of cholesterol lowering (Journal of the American College of Cardiology, 2021). Because it is a complex physiological process rather than a discrete protein or receptor, it is classified as a disease state or mechanism rather than a canonical drug target.

Other names

Vascular inflammationAtheroinflammationEndothelial inflammationChronic vascular inflammation

Therapeutic strategies targeting arterial inflammation involve the inhibition of pro-inflammatory cytokines (e.g., IL-1β by canakinumab), inhibition of the NLRP3 inflammasome and microtubule polymerization (colchicine), reduction of lipid-mediated endothelial activation (statins), and inhibition of cyclooxygenase enzymes (aspirin).