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Sestrin como un inhibidor de la retroalimentación de TOR que previene las patologías relacionadas con la edad
Jun Hee Lee1, Andrei V Budanov, Eek Joong Park
1Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California San Diego (UCSD), La Jolla, CA 92093-0723, USA.
Science (New York, N.Y.)
|March 6, 2010
Resumen
Las estrinas son proteínas que ayudan a las células a responder al estrés. La pérdida de Drosophila sestrin (dSesn) causó enfermedades relacionadas con la edad, pero la activación de AMPK o la inhibición de TOR evitaron estos problemas.
Área de la Ciencia:
- Biología celular Biología celular.
- Biología Molecular Biología Molecular
- Investigación sobre el envejecimiento Investigación sobre el envejecimiento.
Sus antecedentes:
- Las estrinas son proteínas inducidas por el estrés que se sabe que modulan la energía celular y las vías de crecimiento.
- La proteína quinasa activada por monofosfato de adenosina (AMPK) y el objetivo de la rapamicina (TOR) son reguladores clave del metabolismo y el crecimiento celular.
- La activación crónica de TOR está relacionada con varias patologías.
Objetivo del estudio:
- Para investigar el papel de Drosophila sestrin (dSesn) en la respuesta al estrés celular y el envejecimiento.
- Para determinar la relación entre dSesn, la señalización TOR y las patologías asociadas a la edad.
- Explorar intervenciones terapéuticas para las patologías relacionadas con la activación crónica de TOR.
Principales métodos:
- Utilizó Drosophila melanogaster como organismo modelo.
- Manipulación de la abundancia de sestrina y las vías de señalización TOR.
- Evaluar las patologías asociadas a la edad, incluidos los niveles de triglicéridos, la función mitocondrial, la salud muscular y cardíaca.
- Activadores farmacológicos empleados de AMPK e inhibidores de TOR.
Principales resultados:
- La abundancia de dSesn aumentó bajo la activación crónica de TOR, mediada por especies reactivas de oxígeno, c-Jun amino-terminal quinasa y caja de bifurcación O.
- La pérdida de dSesn condujo a patologías asociadas a la edad como la acumulación de triglicéridos, la disfunción mitocondrial y la degeneración de órganos.
- La activación farmacológica de AMPK o la inhibición de TOR mejoraron estas patologías en moscas con deficiencia de DESEN.
Conclusiones:
- dSesn actúa como un regulador de retroalimentación negativa de la señalización TOR.
- dSesn integra señales metabólicas y de estrés para prevenir patologías de la activación crónica de TOR.
- Esta disfunción puede contribuir a las enfermedades relacionadas con la edad al deteriorar los mecanismos de control de calidad celular.
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