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Galdo Bustos

As seen in: Nature, Cell Press
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Articles

Calcium (Ca2+) fluxes at mitochondria-ER contact sites (MERCS) are a new target of senolysis in therapy-induced senescence (TIS) - npj Aging

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By Sandra A. Niño, Galdo Bustos, José M. Villalba, Christian González-Billault, Osman Díaz-Rivera, Sandra Rodríguez-López, José Antonio González-Reyes
| Nature Verified
Abstract Therapy-induced senescence (TIS) alters calcium (Ca²⁺) flux and Mitochondria-ER Contact Sites (MERCS), revealing critical vulnerabilities in senescent cells. In this study, TIS was induced using Doxorubicin and Etoposide, resulting in an increased MERCS contact surface but a significant reduction in ER-mitochondria Ca²⁺ flux. Mechanistically, TIS cells exhibit decreased expression of IP3R isoforms and reduced interaction between type 1 IP3R and VDAC1, impairing Ca²⁺ transfer.
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Selective Vulnerability of Cancer Cells by Inhibition of Ca2+ Transfer from Endoplasmic Reticulum to Mitochondria

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By Marioly Müller, Andrew McNeal, Alenka Lovy, Galdo Bustos, Felix Urra
| Cell Press Verified
Inhibition of InsP3R Activity Creates a Bioenergetic Crisis in Both Tumorigenic and Non-tumorigenic Cell Lines Inhibition of InsP3R Activity Is Toxic, Specifically for Tumorigenic Cells Inhibition of InsP3R Activity Reduces the Proliferative Potential of Cancer Cell Lines XeB Induces Cell Death in Transformed, But Not Isogenic Control, Human Fibroblasts Killing of Cancer Cells by Inhibition of InsP3R Activity Is Mediated by Altered Mitochondrial Function Cell Death Induced by Inhibition of...
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