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Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders

Darren J. Baker, Tobias Wijshake, Tamar Tchkonia, Nathan K. LeBrasseur, Bennett G. Childs, Bart van de Sluis, James L. Kirkland and Jan M. van Deursen ()
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Darren J. Baker: Mayo Clinic College of Medicine
Tobias Wijshake: Mayo Clinic College of Medicine
Tamar Tchkonia: Robert and Arlene Kogod Center on Aging, Mayo Clinic College of Medicine
Nathan K. LeBrasseur: Robert and Arlene Kogod Center on Aging, Mayo Clinic College of Medicine
Bennett G. Childs: Mayo Clinic College of Medicine
Bart van de Sluis: University Medical Center Groningen, Groningen University
James L. Kirkland: Robert and Arlene Kogod Center on Aging, Mayo Clinic College of Medicine
Jan M. van Deursen: Mayo Clinic College of Medicine

Nature, 2011, vol. 479, issue 7372, 232-236

Abstract: Role of cell senescence in ageing Senescent cells accumulate in tissues with age, but it is not known whether they actually cause age-related dysfunction or whether their removal is beneficial. Using a mouse model with a transgene named INK-ATTAC, which allows for the inducible elimination of cells carrying the senescence biomarker p16Ink4a, Baker et al. demonstrate that life-long removal of senescent cells delays the onset of age-related phenotypes. Furthermore, late-life clearance attenuated the progression of already established age-related disorders. This indicates that senescent cells do cause age-related phenotypes and that their removal can prevent or delay age-related tissue dysfunction.

Date: 2011
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DOI: 10.1038/nature10600

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