Calcium (Ca2+) fluxes at Mitochondria-ER Contact Sites (MERCS) are a new target of senolysis in Therapy-Induced Senescence (TIS).

This study investigates the state of calcium (Ca 2+ ) flux and Mitochondria-ER contact sites (MERCS) on Therapy-Induced Senescence (TIS). TIS cells-induced by Doxorubicin and Etoposide increase their MERCS contact surface but exhibit a decreased ER-mitochondria Ca 2+ flux. TIS cells show decreased levels of IP3R isoforms and a decreased interaction between type 1 IP3R isoform and VDAC1. The ER-mitochondria Ca 2+ flux is essential to maintain the viability of senescence cells. Inhibition of ER-mitochondria Ca 2+ flux rise as a new target of senolysis in vitro and in vivo .