Senomorphic Effect Of Genetic And Chemical Partial Reprogramming
Nunez-Quintela, V.; Chantrel, J.; Prados, M. A.; Pedrosa, P.; Lorandi, I.; Lorenzo Rodriguez, L.; Chen, C.; Paredes, R.; Failde-Fiestras, A.; Gonzalez-Perez, D.; Miralles, A.; Da Silva-Alvarez, S.; Lobato-Busto, R.; Gonzalez-Barcia, M.; Alcon, C.; Montero, J.; Marques, P.; Chondronasiou, D.; Pietrocola, F.; Serrano, M.; Kovatcheva, M.; Gomez-Duran, A.; Li, H.; Collado, M.
Show abstract
Partial reprogramming has emerged as a promising strategy to ameliorate aging phenotypes, yet its cellular targets and mechanisms remain poorly defined. Cellular senescence is a central hallmark of aging and a plausible mediator of reprogramming-induced rejuvenation. Here we show that genetic and chemical partial reprogramming act directly on senescent cells without restoring proliferative capacity. OSKM expression or a reduced two-compound regimen, tranylcypromine and RepSox (2c), attenuates senescence-associated secretory activity, restores mitochondrial homeostasis and apoptotic priming, and improves functional and inflammatory parameters in aged mice, establishing senomorphic, identity-preserving reprogramming as a potentially safer aging intervention.
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