Targeting cell senescence to treat organismal ageing and frailty
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.
Date: 31 January 2019, 14:00 (Thursday, 3rd week, Hilary 2019)
Venue: 66 Banbury Road (Wolsey Hall), 66 Banbury Road OX2 6PR
Venue Details: Seminar room
Speaker: Associate Professor Lynne Cox (Nuffield Department of Population Health, University of Oxford)
Organising department: Oxford Institute of Ageing
Organiser: Professor Sarah Harper (Oxford Institute of Population Ageing, University of Oxford)
Organiser contact email address:
Host: Professor Sarah Harper (Oxford Institute of Population Ageing, University of Oxford)
Part of: Ageing Populations: from Cell to Society
Booking required?: Not required
Cost: free
Audience: Public
Editor: Katia Padvalkava