Pathogenesis of Atherosclerosis: A Multifactorial Process
L. Maximilian Buja
Abstract
Atherosclerosis is an inflammatory and immunologically driven response of the vessel wall to chronic, multifactorial, repetitive injury. Endothelial cell dysfunction leads to increased oxidative stress, production of inflammatory cytokines, expression of adhesion molecules, and accumulation of oxidized LDL. Atherosclerotic plaques form as a consequence of endothelial damage, proliferation of modified smooth muscle cells, influx of monocytes and T lymphocytes, unregulated uptake of LDL cholesterol, foam cell formation, and connective tissue deposition. Inflammation is also important in the erosion or rupture of vulnerable plaques leading to clinical complications of atherosclerosis, including CAD or IHD. CAD is a genetically complex disease in which multiple genes influence the progression of atherosclerosis in populations, although CAD can develop due to single-gene mutations in lipid metabolism in some individuals.