bioRxivCell Biology
Calcium (Ca2+) fluxes at Mitochondria-ER Contact Sites (MERCS) are a new target of senolysis in Therapy-Induced Senescence (TIS).
A. Puebla-Huerta, H. Huerta, C. Quezada-Gutierrez, P. Morgado-Caceres, C. Casanova-Canelo, S. Linsambarth, O. Diaz-Rivera, J. A. Lopez-Dominguez, S. Rodriguez-Lopez, G. Bustos, E. Silva-Pavez, A. Lovy, G. Quiroz, C. Gonzalez-Seguel, E. Salas-Huenuleo, M. Kogan, J. Molgo, A. Zakarian, J. M. Villalba, C. Gonzalez-Billault, U. Ahumada-Castro, J. C. Cardenas
Abstract
O_LIThis study investigates the state of calcium (Ca2+) flux and Mitochondria-ER contact sites (MERCS) on Therapy-Induced Senescence (TIS). C_LIO_LITIS cells-induced by Doxorubicin and Etoposide increase their MERCS contact surface but exhibit a decreased ER-mitochondria Ca2+ flux. C_LIO_LITIS cells show decreased levels of IP3R isoforms and a decreased interaction between type 1 IP3R isoform and VDAC1. C_LIO_LIThe ER-mitochondria Ca2+ flux is essential to maintain the viability of senescence cells. C_LIO_LIInhibition of ER-mitochondria Ca2+ flux rise as a new target of senolysis in vitro and in vivo. C_LI
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