Manipulating senescent cells by eliminating them or by modifying their activity has attracted huge interest for its potential to delay or even treat many age-related diseases, and to improve healthy aging. Mitochondria, and in particular their calcium levels, have emerged as key regulators of cellular senescence, cell death and the balance between the two, and might constitute targets for novel strategies to stifle the viability or properties of senescent cells.
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Acknowledgements
We thank B. Manship for critical reading of this manuscript and the ECOS-ANID program for cooperation between France and Chile (D.B. and C.C.). The authors were supported by ANID/FONDECYT #1200255 (C.C.), #1240807 (C.C.), ANID/FONDAP #15150012 (C.C.) and ANID/FONDECYT postdoctoral fellowship #3220593 (U.A.-C.). C.M. is supported by a fellowship from la Ligue Nationale Contre le Cancer. P.M.-C. is supported by ANID Doctoral scholarship.
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All the authors contributed to writing individual parts. D.B. conceptualized this Comment, and modified and compiled all the contributions. All of the authors revised and finalized the manuscript. C.M. drew the original figures with the help of P.M.-C.
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Margand, C., Morgado-Cáceres, P., Ahumada-Castro, U. et al. Emerging role of mitochondrial calcium levels in cellular senescence and in switching cell fates. Nat Aging 5, 1177–1180 (2025). https://doi.org/10.1038/s43587-025-00887-1
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DOI: https://doi.org/10.1038/s43587-025-00887-1
