Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 1 de 1
Filtrar
Añadir filtros








Intervalo de año
1.
Protein & Cell ; (12): 202-216, 2023.
Artículo en Inglés | WPRIM | ID: wpr-982531

RESUMEN

Although the mTOR-4E-BP1 signaling pathway is implicated in aging and aging-related disorders, the role of 4E-BP1 in regulating human stem cell homeostasis remains largely unknown. Here, we report that the expression of 4E-BP1 decreases along with the senescence of human mesenchymal stem cells (hMSCs). Genetic inactivation of 4E-BP1 in hMSCs compromises mitochondrial respiration, increases mitochondrial reactive oxygen species (ROS) production, and accelerates cellular senescence. Mechanistically, the absence of 4E-BP1 destabilizes proteins in mitochondrial respiration complexes, especially several key subunits of complex III including UQCRC2. Ectopic expression of 4E-BP1 attenuates mitochondrial abnormalities and alleviates cellular senescence in 4E-BP1-deficient hMSCs as well as in physiologically aged hMSCs. These f indings together demonstrate that 4E-BP1 functions as a geroprotector to mitigate human stem cell senescence and maintain mitochondrial homeostasis, particularly for the mitochondrial respiration complex III, thus providing a new potential target to counteract human stem cell senescence.


Asunto(s)
Humanos , Células Madre Mesenquimatosas/fisiología , Senescencia Celular , Homeostasis , Proteínas de Ciclo Celular/metabolismo , Proteínas Adaptadoras Transductoras de Señales/metabolismo , Mitocondrias/metabolismo , Complejo III de Transporte de Electrones/metabolismo , Células Cultivadas
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA