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Vol. 58. Núm. 1.
Páginas 51-56 (Enero 2006)
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Vol. 58. Núm. 1.
Páginas 51-56 (Enero 2006)
DOI: 10.1016/S0003-3170(06)74949-5
Acceso a texto completo
Participación de la lipoproteína de baja densidad oxidada en el desarrollo de la placa ateroesclerótica
The role played by oxidised low-density lipo protein in the development of the atherosclerotic plaque
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M. Vega de Céniga
Autor para correspondencia
mvega@hgda.osakidetza.net

Correspondencia: Servicio de Angiología y Cirugía Vascular. Hospital de Galdakao. Barrio Labeaga, s/n. E-48960 Galdakao (Vizcaya). Fax: +34 944 007132.
Servicio de Angiología y Cirugía Vascular. Hospital de Galdakao. Galdakao, Vizcaya, España
Información del artículo
Resumen
Bibliografía
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Estadísticas
Resumen
Objetivo

Exponer cuáles son los mecanismos por los cuales los lípidos plasmáticos, y concretamente la lipoproteína de baja densidad (LDL) oxidada, contribuyen al desarrollo de la placa ateromatosa.

Desarrollo

La disfunción endotelialy la formación de la estría grasa constituyen la etapa inicial en el desarrollo de la arterioesclerosis. La hipercoleste-rolemia favorece la oxidación de LDL en contacto con radicales libres de oxígeno liberados por células endoteliales, macrófagos y células musculares lisas, y su captación y acumulación incontrolada por macrófagos subendoteliales, que se transforman en células espumosas. El acúmulo de estas células, con un leve engrosamiento intimal, constituye la estría grasa. La LDL oxidada estimula la quimiotaxis de células inflamatorias, su adhesión a células endoteliales y su migración al interior de la pared vascular; además, promueve la proliferación de células musculares lisas y su infiltración en el espacio subintimal; induce la apoptosis en el núcleo de la placa, favorece un estado protrombótico y reduce la función fibrinolítica. Así, participa en la progresión de las lesiones hacia placas ateromatosas bien estructuradas. La aplicación terapéutica de suplementos dietéticos de antioxidantes y –más importante en la actualidad– la administración de estatinas pueden retrasar la progresión de lesiones arterioescleróticas.

Conclusiones

La hipercolesterolemia, a través de la LDL oxidada, ejerce un papel fundamental en el proceso de la aterogénesis. El conocimiento de su mecanismo de actuación es importante para el cirujano vascular, ya que supone una eficaz diana terapéutica. [ANGIOLOGÍA 2006; 58: 51-6]

Palabras clave:
Antioxidantes
Arterioesclerosis
Estatinas
Estría grasa
Inflamación
LDL oxidada
Summary
Aim

To present how plasma lipids, and particularly oxidized low-density lipoprotein (LDL), participate in the development of the atheromatous plaque.

Development

Endotelial dysfunction and the development of fatty streaks are the initial events in the process of plaque formation. Hypercholesterolemia favours the oxidation of LDL in contact with oxygen-derived free radicals released by endothelial cells, macrophages and smooth muscle cells, and their uncontrolled uptake and accumulation by subendothelial macrophages, which turn into foam cells. The accumulation of these cells, together with a slight intimal thickening, makes up the fatty streak. The oxidized LDL stimulates the chemo-attraction of inflammatory cells, their adhesion to endothelial cells and their migration into the structure of the vascular wall. It promotes the proliferation of smooth muscle cells and their infiltration into the subintimal space. It induces cell apoptosis in the core of the plaque, and it favours a prothrombotic state by reducing the fibrinolytic activity. Thus, it participates in the progression of the vascular lesions towards well-structured atheromatous plaques. The therapeutic application of diet supplements of antioxidants or, more important nowadays, the prescription of statins, can slow down the progression of atherosclerotic lesions.

Conclusions

Hypercholesterolemia, by means of the oxidized LDL, plays an essential role in the atherosclerotic development. It is important for the vascular surgeon to be familiar with this process because it is an effective therapeutic target. [ANGIOLOGÍA 2006; 58: 51-6]

Key words:
Antioxidants
Atherosclerosis
Fatty streak
Inflammation
Oxidized LDL
Statins
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Copyright © 2006. SEACV
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