Mitochondrial dysfunction and cell senescence: deciphering a complex relationship

James Chapman, Edward Fielder, Joao Passos

Research output: Contribution to journalReview article

5 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1566-1579
Number of pages14
JournalFEBS Letters
Volume593
Issue number13
DOIs
StatePublished - Jul 1 2019

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Keywords

  • ageing
  • mitochondria
  • senescence
  • senolytics
  • senostatics

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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