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El desequilibrio de las proteínas mitonucleares como mecanismo de conservación de la longevidad
Riekelt H Houtkooper1, Laurent Mouchiroud, Dongryeol Ryu
1Laboratory for Integrative and Systems Physiology, Ecole Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland.
Nature
|May 24, 2013
Resumen
Las proteínas ribosómicas mitocondriales (MRPs) regulan la longevidad controlando el equilibrio entre las proteínas nucleares y mitocondriales. La alteración de este equilibrio activa una vía clave de longevidad conservada en todas las especies.
Área de la Ciencia:
- Biología celular Biología celular.
- Genética La genética.
- Investigación sobre el envejecimiento Investigación sobre el envejecimiento
Sus antecedentes:
- La longevidad está influenciada por las vías metabólicas interconectadas.
- La función mitocondrial juega un papel crítico en la regulación del envejecimiento y la esperanza de vida.
Objetivo del estudio:
- Identificar los reguladores clave del metabolismo y la longevidad.
- Para investigar el papel de las proteínas ribosómicas mitocondriales (MRPs) en el envejecimiento.
Principales métodos:
- Genética de la población de ratones y interferencia del ARN en Caenorhabditis elegans.
- Manipulación farmacológica con antibióticos y bromuro de etidio.
- Análisis del desequilibrio de la proteína mitonuclear y la respuesta de la proteína desplegada mitocondrial (UPRmt).
Principales resultados:
- La proteína ribosómica mitocondrial S5 (Mrps5) y otros MRPs fueron identificados como reguladores de la longevidad.
- La eliminación de los MRPs indujo un desequilibrio de la proteína mitonuclear, redujo la respiración y activó la UPRmt.
- Los antibióticos, el bromuro de etidio, el resveratrol y la rapamicina imitaron los efectos de eliminación de la MRP, extendiendo la vida útil al inducir el desequilibrio mitonuclear y la UPRmt.
Conclusiones:
- Los MRPs son reguladores evolutivamente conservados que vinculan los ribosomas mitocondriales a las vías de longevidad.
- El desequilibrio de la proteína mitonuclear y la UPRmt son mecanismos conservados de extensión de la vida útil.
- Dirigirse a la traducción y transcripción mitocondriales puede modular el envejecimiento.
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