Cellular senescence

Unravelling complexity

João F. Passos, Cedric Simillion, Jennifer Hallinan, Anil Wipat, Thomas Von Zglinicki

Research output: Contribution to journalReview article

31 Citations (Scopus)

Abstract

Cellular senescence might be a tumour suppressing mechanism as well as a contributor to age-related loss of tissue function. It has been characterised classically as the result of the loss of DNA sequences called telomeres at the end of chromosomes. However, recent studies have revealed that senescence is in fact an intricate process, involving the sequential activation of multiple cellular processes, which have proven necessary for the establishment and maintenance of the phenotype. Here, we review some of these processes, namely, the role of mitochondrial function and reactive oxygen species, senescence-associated secreted proteins and chromatin remodelling. Finally, we illustrate the use of systems biology to address the mechanistic, functional and biochemical complexity of senescence.

Original languageEnglish
Pages (from-to)353-363
Number of pages11
JournalAge
Volume31
Issue number4
DOIs
Publication statusPublished - Dec 2009
Externally publishedYes

Keywords

  • Interactomes
  • Mitochondria
  • Oxidative stress
  • Secretory phenotype
  • Senescence
  • Systems biology

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    Passos, J. F., Simillion, C., Hallinan, J., Wipat, A., & Von Zglinicki, T. (2009). Cellular senescence: Unravelling complexity. Age, 31(4), 353-363. https://doi.org/10.1007/s11357-009-9108-1