Lipoproteínas, plaquetas y aterotrombosis

Atherosclerosis and thrombosis associated with the rupture of vulnerable plaque are the main causes of cardiovascular events, including acute coronary syndrome. Low-density lipoprotein (LDL) plays a key role in the pathogenesis of atherothrombotic processes. LDLs modify the antithrombotic properties of the vascular endothelium and change vessel contractility by reducing the availability of endothelial nitric oxide and activating proinflammatory signaling pathways. In addition, LDLs also influence the functions and interactions of cells present in atherosclerotic lesions, whether they come from the circulation or are resident in vessel walls. In fact, LDLs entering affected vessels undergo modifications (e.g. oxidation, aggregation and glycosylation) that potentiate their atherogenic properties. Once modified, these intravascular LDLs promote the formation of foam cells derived from smooth muscle cells and macrophages, thereby increasing the vulnerability of atherosclerotic plaque. Moreover, they also increase the thrombogenicity of both plaque and blood, in which circulating tissue factor levels are raised and platelet reactivity is enhanced. This review focuses on the importance of native and modified LDL for the pathogenesis of atherothrombosis. It also discusses current studies on LDL and its effects on the actions of vascular cells and blood cells, particularly platelets, and considers novel potential therapeutic targets.