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Involucramiento de CD95/Apo1/Fas en la muerte celular después de isquemia miocárdica
I Jeremias1, C Kupatt, A Martin-Villalba
1German Cancer Research Center, Heidelberg, Germany.
Circulation
|August 23, 2000
Resumen
La muerte celular cardíaca después de la isquemia / reperfusión implica apoptosis. El sistema CD95, incluido el ligando CD95, juega un papel directo en este proceso, lo que lo sugiere como un objetivo terapéutico para la recuperación del ataque cardíaco.
Área de la Ciencia:
- Biología Cardiovascular Biología Cardiovascular
- Mecanismos de muerte celular Mecanismos de muerte celular
- Cardiología Molecular Cardiología Molecular
Sus antecedentes:
- La muerte celular cardíaca después de la isquemia y la lesión por reperfusión es una preocupación clínica significativa.
- La apoptosis, una vía de muerte celular programada, contribuye al daño miocárdico después del infarto agudo de miocardio.
Objetivo del estudio:
- Investigar el papel específico del sistema de receptores CD95/Fas/Apo1 en la mediación de la muerte celular cardíaca posisquémica.
- Explorar la participación del ligando CD95 y otros ligandos que inducen la muerte en el contexto de la isquemia miocárdica-reperfusión.
Principales métodos:
- Se utilizó un modelo de perfusión de Langendorff de corazón aislado de rata y ratón para simular isquemia-reperfusión.
- Se evaluó la apoptosis caspase-dependiente y la liberación/síntesis del ligando CD95 y otros ligandos de muerte (TNF-alfa, TRAIL).
- Se examinó la sensibilidad de los miocitos primarios de rata adulta al ligando CD95 bajo hipoxia / reoxigenación y se comparó la muerte celular en ratones con deficiencia de CD95 (lpr) frente a controles de tipo salvaje.
Principales resultados:
- La reperfusión posisquémica en corazones aislados indujo la apoptosis caspase-dependiente.
- El ligando soluble CD95 fue liberado y sintetizado de novo por los corazones post-isquémicos, junto con TNF-alfa y TRAIL.
- La hipoxia / reoxigenación aumentó la sensibilidad de los miocitos al ligando CD95, y los corazones con deficiencia de CD95 mostraron una reducción de la muerte celular después de la isquemia-reperfusión.
Conclusiones:
- El sistema CD95/Apo1/Fas está directamente implicado en la muerte celular cardíaca después de la isquemia miocárdica.
- La vía de señalización CD95 presenta un potencial nuevo objetivo terapéutico para prevenir la muerte celular en el corazón después de eventos isquémicos.
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