Journal
CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 74, Issue 24, Pages 4471-4509Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00018-017-2587-9
Keywords
Keratinocytes; Mammary epithelial cells; SASP; DNA damage; DSB; SSB; p16; p38MAPK; p53; PARP1; Oxidative stress; Proteostasis; Unfolded protein response; Autophagy; Aging; Cancer
Categories
Funding
- Centre National de la Recherche Scientifique
- Universite Lille 1
- Universite Lille 2
- Ligue contre le Cancer (Comite du Pas-de-Calais)
- Ligue contre le Cancer (Comite de la Somme)
- Institut Pasteur de Lille
- SIRIC OncoLille [INCa-DGOS-Inserm 6041]
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Senescence is a cell state occurring in vitro and in vivo after successive replication cycles and/or upon exposition to various stressors. It is characterized by a strong cell cycle arrest associated with several molecular, metabolic and morphologic changes. The accumulation of senescent cells in tissues and organs with time plays a role in organismal aging and in several age-associated disorders and pathologies. Moreover, several therapeutic interventions are able to prematurely induce senescence. It is, therefore, tremendously important to characterize in-depth, the mechanisms by which senescence is induced, as well as the precise properties of senescent cells. For historical reasons, senescence is often studied with fibroblast models. Other cell types, however, much more relevant regarding the structure and function of vital organs and/or regarding pathologies, are regrettably often neglected. In this article, we will clarify what is known on senescence of epithelial cells and highlight what distinguishes it from, and what makes it like, replicative senescence of fibroblasts taken as a standard.
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