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 ()
Additional contact information
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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Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:479:y:2011:i:7372:d:10.1038_nature10600
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DOI: 10.1038/nature10600
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