Inflammation and Atherosclerosis

Atherosclerosis is a slowly progressing disorder of large- and medium-sized arteries leading to overt disease when significant narrowing or atherosclerotic plaque rupture occurs. Inflammation plays a key role in atherosclerotic plaque formation, progression and rapture. Both innate and adaptive immune responses are important to disease pathogenesis. Toll-like receptors, NOD-like receptors and the inflammasome are key components of LDL and other atherogenic molecule recognition and internalization and the subsequent interaction with components of the adaptive immune response. The NLPR3 inflammasome acts through the activation of caspase, can be primed by TLR activation and seems to have a crucial role in atherosclerosis and other related disorders such as diabetes, obesity and the metabolic syndrome. However, its experimental inactivation/modification has provided conflicting results in animal models of the disease. Lipid perturbations are also important since they can lead to endothelial cell activation and the augmentation of the inflammatory immune response; even high density lipoproteins may lose their atheroprotective capacities. Chronic inflammatory diseases are characterized by accelerated atherosclerosis: Systemic lupus erythematosus, rheumatoid arthritis, Sjogren syndrome and antiphospholipid syndrome patients display an increased incidence of cardiovascular disease not explained by traditional risk factors.