Cellular senescence: unravelling complexity.
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.
Passos
João F
JF
Ageing Biology Laboratories and Centre for Integrated Systems Biology of Ageing and Nutrition (CISBAN), Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, UK. Joao.Passos@ncl.ac.uk
Simillion
Cedric
C
Hallinan
Jennifer
J
Wipat
Anil
A
von Zglinicki
Thomas
T
D000375:Aging / Q000502:physiology*; D000818:Animals; D016922:Cellular Senescence / Q000502:physiology*; D004249:DNA Damage; D006801:Humans; D008928:Mitochondria / Q000235:genetics* / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism*; D016615:Telomere / Q000378:metabolism*
D017382:Reactive Oxygen Species