Cellular senescence: Unravelling complexity

Joao Passos, Cedric Simillion, Jennifer Hallinan, Anil Wipat, Thomas Von Zglinicki

Research output: Contribution to journalReview article

28 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 (US)
Pages (from-to)353-363
Number of pages11
JournalAge
Volume31
Issue number4
DOIs
StatePublished - Dec 1 2009
Externally publishedYes

Fingerprint

Cell Aging
Chromatin Assembly and Disassembly
Systems Biology
Telomere
Reactive Oxygen Species
Chromosomes
Maintenance
Phenotype
Neoplasms
Proteins

Keywords

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

ASJC Scopus subject areas

  • Aging
  • Geriatrics and Gerontology

Cite this

Passos, J., 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

Cellular senescence : Unravelling complexity. / Passos, Joao; Simillion, Cedric; Hallinan, Jennifer; Wipat, Anil; Von Zglinicki, Thomas.

In: Age, Vol. 31, No. 4, 01.12.2009, p. 353-363.

Research output: Contribution to journalReview article

Passos, J, Simillion, C, Hallinan, J, Wipat, A & Von Zglinicki, T 2009, 'Cellular senescence: Unravelling complexity', Age, vol. 31, no. 4, pp. 353-363. https://doi.org/10.1007/s11357-009-9108-1
Passos J, Simillion C, Hallinan J, Wipat A, Von Zglinicki T. Cellular senescence: Unravelling complexity. Age. 2009 Dec 1;31(4):353-363. https://doi.org/10.1007/s11357-009-9108-1
Passos, Joao ; Simillion, Cedric ; Hallinan, Jennifer ; Wipat, Anil ; Von Zglinicki, Thomas. / Cellular senescence : Unravelling complexity. In: Age. 2009 ; Vol. 31, No. 4. pp. 353-363.
@article{8af5955f6a804d64a944e1101d7a0667,
title = "Cellular senescence: Unravelling complexity",
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.",
keywords = "Interactomes, Mitochondria, Oxidative stress, Secretory phenotype, Senescence, Systems biology",
author = "Joao Passos and Cedric Simillion and Jennifer Hallinan and Anil Wipat and {Von Zglinicki}, Thomas",
year = "2009",
month = "12",
day = "1",
doi = "10.1007/s11357-009-9108-1",
language = "English (US)",
volume = "31",
pages = "353--363",
journal = "GeroScience",
issn = "2509-2715",
publisher = "Springer International Publishing AG",
number = "4",

}

TY - JOUR

T1 - Cellular senescence

T2 - Unravelling complexity

AU - Passos, Joao

AU - Simillion, Cedric

AU - Hallinan, Jennifer

AU - Wipat, Anil

AU - Von Zglinicki, Thomas

PY - 2009/12/1

Y1 - 2009/12/1

N2 - 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.

AB - 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.

KW - Interactomes

KW - Mitochondria

KW - Oxidative stress

KW - Secretory phenotype

KW - Senescence

KW - Systems biology

UR - http://www.scopus.com/inward/record.url?scp=75949094234&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=75949094234&partnerID=8YFLogxK

U2 - 10.1007/s11357-009-9108-1

DO - 10.1007/s11357-009-9108-1

M3 - Review article

C2 - 19618294

AN - SCOPUS:75949094234

VL - 31

SP - 353

EP - 363

JO - GeroScience

JF - GeroScience

SN - 2509-2715

IS - 4

ER -