'Targeting cell senescence to treat organismal ageing and frailty' with Prof Lynne Cox

Past Event

31 January 2019, 3:00pm - 4:30pm

Oxford Institute of Population Ageing
66 Banbury Road, Oxford, OX2 6PR

This seminar is organised by the Oxford Institute of Population Ageing

As organisms (and people) age, their cells gradually accumulate changes that eventually trigger a stress response pathway known as cellular senescence. Senescent cells show many specific features that are now recognised to be hallmarks of ageing. In particular, they lose the ability to undergo self-renewal (cell division), leading to an inability to replenish tissue or contribute to wound healing. Such cells also change their patterns to gene expression and produce a number of secreted factors that lead to a state of chronic inflammation and tissue damage, creating a pro-tumorigenic environment. Experimental removal of senescent cells in middle aged and even old mice leads to quite marked rejuvenation, while transplanting senescent cells into young animals leads to premature ageing. Such findings are powerful indicators that cell senescence is both necessary and sufficient to drive organismal ageing. I will discuss current approaches to deal with senescent cells, including cutting edge clinical trials to remove senescent cells in people, as well as work from my own lab where we have reversed many deleterious features of human cell ageing by targeting specific biochemical pathways we have identified in longitudinal cell ageing studies.

All are welcome, no need to register to attend. Join us for coffee and cake afterwards.

For queries please contact: administrator@ageing.ox.ac.uk

About the speaker

Professor Lynne Cox is George Moody Fellow and Tutor in Biochemistry, Nuffield Department of Population Health. Professor Cox’s team studies the molecular basis of human ageing, with the aim of reducing the morbidity and frailty associated with old age.


  • Ageing, biological basis and molecular mechanisms
  • Cell ageing
  • Premature ageing syndromes
  • DNA replication