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Trends Mol Med. 2014 Dec;20(12):667-74. doi: 10.1016/j.molmed.2014.09.008. Epub 2014 Sep 30.

Ageing as developmental decay: insights from p16(INK4a.).

Author information

1
Cell Proliferation Group, Medical Research Council (MRC) Clinical Sciences Centre, Imperial College London, Hammersmith Campus, London W12 0NN, UK.
2
Blizard Institute of Cell and Molecular Science, Barts and The London School of Medicine and Dentistry, London E1 2AT, UK. Electronic address: dhbeach@btinternet.com.
3
Cell Proliferation Group, Medical Research Council (MRC) Clinical Sciences Centre, Imperial College London, Hammersmith Campus, London W12 0NN, UK. Electronic address: jesus.gil@csc.mrc.ac.uk.

Abstract

The p16(INK4a) cell cycle regulator is one of the best ageing biomarkers because it is suppressed in early embryogenesis and progressively induced during ageing. p16(INK4a) plays a crucial role in key cell fate decisions which contribute to ageing, such as cellular senescence and stem cell dynamics. Detailed examination of the pathways regulating p16(INK4a) expression has revealed an overlap with those regulating early development. We present the hypothesis that ageing might be primarily driven by gradual functional decay of developmental pathways. To support this, we summarise the role of p16(INK4a) in ageing and our current knowledge on p16(INK4a) regulation. The developmental decay hypothesis implies that the much-evidenced damage associated with all aspects of ageing might be secondary to such decay.

KEYWORDS:

ageing; development; p16(INK4a); senescence

PMID:
25277993
DOI:
10.1016/j.molmed.2014.09.008
[Indexed for MEDLINE]
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