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Updated: Dec 8, 2025

In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells
Published on: June 12, 2017
A bidirectional crosstalk between autophagy and TP53 determines the pace of aging
Valentina Sica1,2,3, Guido Kroemer1,2,4,5,6
1Centre De Recherche Des Cordeliers, Equipe Labellisée Par La Ligue Contre Le Cancer, Université De Paris, Sorbonne Université, Inserm, Paris, France.
Abstract:
When the orthologue of tumor suppressor protein p53 (TP53), cep-1, is inactivated in Caenorhabditis elegans, the nematodes manifest an autophagy-dependent increase in lifespan. A recent paper by Yang et al. demonstrates that accelerated aging phenotype of autophagy-deficient mice can be reduced by the knockout (KO) of Trp53. These findings point to a complex bidirectional crosstalk between autophagy and TP53 that has vast implications for the aging process.
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