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Las estatinas tienen efectos bifásicos en la angiogénesis.

Michael Weis1, Christopher Heeschen, Alec J Glassford

  • 1Stanford University School of Medicine, Division of Cardiovascular Medicine, Stanford, Calif 94305, USA.

Circulation
|February 13, 2002
PubMed
Resumen

Las estatinas exhiben un doble efecto en la formación de vasos sanguíneos (angiogénesis). Las dosis bajas lo promueven, mientras que las dosis altas lo inhiben al afectar las células endoteliales y los factores de crecimiento vascular, independientemente de los niveles de colesterol.

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Área de la Ciencia:

  • La bioquímica es la bioquímica.
  • Biología celular Biología celular.
  • Farmacología Farmacología.

Sus antecedentes:

  • Las estatinas son inhibidores de la HMG-CoA reductasa, que afectan el colesterol y la síntesis de isoprenoides.
  • Los isoprenoides regulan varias funciones celulares, incluida la angiogénesis.
  • Se investigaron los efectos de la cerivastatina y la atorvastatina en la angiogénesis.

Objetivo del estudio:

  • Para investigar los efectos dependientes de la dosis de las estatinas en la angiogénesis.
  • Para determinar si estos efectos son dependientes de los lípidos.
  • Para explorar el papel del pirofosfato de geranilgeranil en la angiogénesis mediada por estatinas.

Principales métodos:

  • Estudios in vitro con el uso de células endoteliales (proliferación, migración, diferenciación).
  • Estudios in vivo en modelos murinos de angiogénesis inducida por la inflamación.
  • Evaluación del crecimiento tumoral y la vascularización en un modelo de cáncer de pulmón de Lewis.

Principales resultados:

  • Las bajas concentraciones de estatinas (0,005-0,01 μmol/L) mejoran las funciones de las células endoteliales.
  • Las altas concentraciones de estatinas (0,05-1 μmol/L) inhiben la angiogénesis, disminuyen el factor de crecimiento endotelial vascular (VEGF) y aumentan la apoptosis endotelial.
  • Las estatinas en dosis altas inhibieron la angiogénesis inducida por la inflamación y el crecimiento tumoral en ratones, efectos revertidos por el pirofosfato de geranilgeranilo.

Conclusiones:

  • La inhibición de la HMG-CoA reductasa tiene un efecto bifásico y dependiente de la dosis en la angiogénesis.
  • Los efectos de las estatinas en la angiogénesis son independientes de los lípidos y están relacionados con la apoptosis endotelial y la señalización VEGF.
  • Las dosis bajas de estatinas terapéuticas pueden ser proangiogénicas, mientras que las dosis altas son angiostáticas, afectando a las proteínas geraniladas.