Abstract

Recent data suggest that we age, in part, because our self-renewing stem cells grow old as a result of heritable intrinsic events, such as DNA damage, as well as extrinsic forces, such as changes in their supporting niches. Mechanisms that suppress the development of cancer, such as senescence and apoptosis, which rely on telomere shortening and the activities of p53 and p16^INK4a, may also induce an unwanted consequence: a decline in the replicative function of certain stem-cell types with advancing age. This decreased regenerative capacity appears to contribute to some aspects of mammalian ageing, with new findings pointing to a 'stem-cell hypothesis' for human age-associated conditions such as frailty, atherosclerosis and type 2 diabetes.

Author affiliations

1. Departments of Medicine and Genetics, The Lineberger Comprehensive Cancer Center, The University of North Carolina, Chapel Hill, North Carolina 27599-7295, USA.
   Email: nes@med.unc.edu
2. Center for Applied Cancer Science of the Belfer Institute for Innovative Cancer Science, and Department of Medical Oncology, Dana-Farber Cancer Institute; Departments of Medicine and Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA.
   Email: ron_depinho@dfci.harvard.edu

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