Resumen

PORTILLA, Eliana C; MUNOZ, Wilson  y  SIERRA, Carlos H. Cellular and molecular mechanisms of atherothrombosis. Rev. Colomb. Cardiol. [online]. 2014, vol.21, n.1, pp.35-43. ISSN 0120-5633.

Atherosclerosis results from an altered arterial endothelial function, triggered by the continuous exposure of this tissue to turbulent circulatory phenomena. The presence of cardiovascular risk factors promotes the overexpression of proinflammatory molecules that initiate the inflammatory cascade within the vessel. Once immune cells such as monocytes and macrophages have entered the artery, these initiate a series of events that include the internalization of lipid particles in the macrophage and the formation of foam cells and fatty streaks. Subsequently, the inflammatory response is exacerbated and the lipid core formation and development of atheromatous plaque continues. The inflammatory process modulates the overexpression of prothrombotic mechanisms that act in response to the rupture or erosion of the atherosclerotic plaque and triggers thrombotic or embolic events. The aim of this review is to present evidence about the cellular and molecular mechanisms involved in the processes of endothelial dysfunction, inflammation and thrombosis that underlie the initiation and progression of atherosclerosis.

Palabras clave : oxidative stress; endothelial dysfunction; inflammation; coagulation; atherosclerosis; cardiovascular disease.

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