Lookup NU author(s): James Chapman,
Dr Joao Passos
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
© 2019 Federation of European Biochemical Societies. Cellular senescence and mitochondrial dysfunction have both been defined as classical hallmarks of the ageing process. Here, we review the intricate relationship between the two. In the context of ageing, it is now well regarded that cellular senescence is a key driver in both ageing and the onset of a number of age-related pathologies. Emerging evidence has pinpointed mitochondria as one of the key modulators in the development of the senescence phenotype, particularly the pro-inflammatory senescence associated secretory phenotype (SASP). This review focuses on the contribution of homeostatic mechanisms, as well as of reactive oxygen species and mitochondrial metabolites in the senescence programme. Furthermore, we discuss emerging pathways and mitochondrial-mediated mechanisms that may be influencing the SASP and, subsequently, explore how these may be exploited to open up new therapeutic avenues.
Author(s): Chapman J, Fielder E, Passos JF
Publication type: Review
Publication status: Published
Journal: FEBS Letters
Print publication date: 01/07/2019
Online publication date: 27/06/2019
Acceptance date: 13/06/2019
ISSN (print): 0014-5793
ISSN (electronic): 1873-3468
Publisher: Wiley Blackwell