Vascular inflammation

Vascular inflammation is a complex biological process characterized by the activation of endothelial cells and the subsequent recruitment of leukocytes to the blood vessel wall. It is not a single molecular target, but rather a pathological state central to the development and progression of atherosclerosis, vasculitis, and other cardiovascular diseases (Source: AHA, Circulation Research, 2016). The process is initiated by various stimuli, including oxidized lipids, hemodynamic stress, and cytokines, which trigger the expression of adhesion molecules like VCAM-1 and pro-inflammatory signaling via IL-1 beta and TNF-alpha. Chronic inflammation leads to the formation of fibrofatty plaques that are prone to rupture, potentially resulting in myocardial infarction or stroke (Source: StatPearls, Inflammation). While the term describes a broad disease process, specific components of the pathway are targeted by drugs like statins, which exert pleiotropic anti-inflammatory effects, or monoclonal antibodies like canakinumab, which specifically inhibits the IL-1 beta pathway (Source: PubMed, PMID: 28859337). Managing vascular inflammation is a key therapeutic strategy for reducing residual cardiovascular risk in patients who have already achieved target cholesterol levels. It is typically monitored in clinical practice using biomarkers like high-sensitivity C-reactive protein (hs-CRP).

Other names

VasculitisEndothelial inflammationAngiitisVessel wall inflammation

As vascular inflammation is a physiological process rather than a single molecule, drugs affect it by inhibiting specific molecular nodes within the inflammatory cascade, such as blocking interleukin-1 beta (IL-1 beta) signaling, inhibiting HMG-CoA reductase to reduce endothelial activation, or interfering with microtubule polymerization in leukocytes (Source: Nature Reviews Cardiology, 2019; NIH, PMC5482787).