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Represión transcripcional de la inflamación aterogénica: modulación por el PPARdelta
Chih-Hao Lee1, Ajay Chawla, Ned Urbiztondo
1Howard Hughes Medical Institute, Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.
Science (New York, N.Y.)
|September 13, 2003
Resumen
El receptor activado por el proliferador peroxisomático (PPAR) delta, no gamma, controla la inflamación en las células de espuma. La eliminación de PPARdelta en las células de espuma redujo significativamente el área de la lesión aterosclerótica, lo que lo sugiere como un objetivo terapéutico.
Área de la Ciencia:
- Biología cardiovascular Biología cardiovascular
- Los mecanismos moleculares de la aterosclerosis
- Inflamación y inmunidad.
Sus antecedentes:
- La formación de lesiones ateroscleróticas implica macrófagos cargados de lípidos (células de espuma) y inflamación crónica.
- El receptor gamma activado por el proliferador peroxisomático (PPAR) influye en el metabolismo de los lípidos en las células de espuma.
- El papel del receptor PPARdelta relacionado en la inflamación de los macrófagos no estaba claro.
Objetivo del estudio:
- Investigar el papel de PPARdelta en la regulación del estado inflamatorio de los macrófagos dentro de las lesiones ateroscleróticas.
- Para determinar si PPARdelta influye en la progresión de la lesión aterosclerótica.
Principales métodos:
- Utilizó la deleción genética de PPARdelta específicamente en células de espuma.
- Se evaluó el impacto de la deleción de PPARdelta en los marcadores inflamatorios y el tamaño de la lesión aterosclerótica.
- Investigó los mecanismos reguladores de la transcripción que involucran a los PPARdelta.
Principales resultados:
- La eliminación de PPARdelta en las células de espuma condujo a una reducción significativa (más del 50%) en el área de la lesión aterosclerótica.
- La deleción del PPARdelta aumentó la disponibilidad de supresores inflamatorios dentro de los macrófagos.
- Se identificó una vía transcripcional dependiente de ligandos en la que el PPARdelta modula la inflamación a través de interacciones con represores transcripcionales.
Conclusiones:
- PPARdelta, no PPAR gamma, juega un papel crítico en el control del estado inflamatorio de los macrófagos en la aterosclerosis.
- Dirigirse a PPARdelta y sus ligandos puede ofrecer una nueva estrategia terapéutica para reducir la inflamación y retrasar la progresión de la aterosclerosis.
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