From the Hayflick mosaic to the mosaics of ageing. Role of stress-induced premature senescence in human ageing

Olivier Toussaint, Jose Remacle, Jean François Dierick, Thierry Pascal, Christophe Frippiat, Stéphanie Zdanov, Joao Pedro Magalhaes, Véronique Royer, Florence Chainiaux

Research output: Contribution to journalArticlepeer-review


The Hayflick limit - senescence of proliferative cell types - is a fundamental feature of proliferative cells in vitro. Various human proliferative cell types exposed in vitro to many types of subcytotoxic stresses undergo stress-induced premature senescence (SIPS) (also called stress-induced premature senescence-like phenotype, according to the definition of senescence). The known mechanisms of appearance the main features of SIPS are reviewed: senescent-like morphology, growth arrest, senescence-related changes in gene expression, telomere shortening. Long before telomere-shortening induces senescence, other factors such as culture conditions or lack of 'feeder cells' can trigger either SIPS or prolonged reversible G0 phase of the cell cycle. In vivo, 'proliferative' cell types of aged individuals are likely to compose a mosaic made of cells irreversibly growth arrested or not. The higher level of stress to which these cells have been exposed throughout their life span, the higher proportion of the cells of this mosaic will be in SIPS rather than in telomere-shortening dependent senescence. All cell types undergoing SIPS in vivo, most notably the ones in stressful conditions, are likely to participate in the tissular changes observed along ageing. For instance, human diploid fibroblasts (HDFs) exposed in vivo and in vitro to pro-inflammatory cytokines display biomarkers of senescence and might participate in the degradation of the extracellular matrix observed in ageing. © 2002 Elsevier Science Ltd. All rights reserved.

Original languageEnglish
Pages (from-to)1415-1429
Number of pages15
JournalThe international journal of Biochemistry & Cell biology
Issue number11
Publication statusPublished - 1 Nov 2002


  • Ageing
  • Apolipoprotein J
  • Oxidative stress
  • Senescence
  • Telomeres
  • TGF-β1


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