Timing-Dependent Clearance of p16-Positive Cells Mitigates Radiation-Induced Accelerated Aging.

Karla Valdivieso, Melanie Weigand, Daniela G Costa, Gung Lee, Nick Pirius, Helene Martini, Shivangi Oberai, Christina Inman, Yi Zhu, Thomas von Zglinicki, Sundeep Khosla, Nathan LeBrasseur, João F Passos, Tamara Tchkonia, James L Kirkland, Diana Jurk

Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA. · pubmed

Paper

Abstract

Genotoxic stress induced by cancer therapies is increasingly recognized as a driver of accelerated aging in long-term cancer survivors, yet the mechanisms responsible for the emergence of age-related dysfunction months to years after treatment remain poorly understood. Here, we use sublethal whole-body irradiation as a model of systemic genotoxic stress to test whether senescent cells contribute to the progression of post-therapy age-related dysfunction and whether the benefits of senescent cell clearance depend on the timing of intervention. Using the INK-ATTAC mouse model, we selectively eliminated p16

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Research summary

The paper claims that the timing of senescent cell clearance is critical for mitigating radiation-induced accelerated aging, with early intervention being more effective than late intervention. This is relevant because it investigates the mechanism of senescence as a driver of age-related dysfunction and tests a specific intervention (senolytics) to prevent the acceleration of the aging process, rather than just treating the symptoms of a specific disease.

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