Cellular Senescence in Postmitotic Cells: Beyond Growth Arrest
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Updated: Feb 11, 2026

Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
Przemyslaw Sapieha1, Frédérick A Mallette2
1Département de Biochimie et Médecine Moléculaire, C.P. 6128, Succ. Centre-Ville, Montréal, QC, H3C 3J7, Canada; Département d'Ophtalmologie, Université de Montréal, C.P. 6128, Succ. Centre-Ville, Montréal, QC, H3C 3J7, Canada; Maisonneuve-Rosemont Hospital Research Centre, Montréal, QC, H1T 2M4, Canada.
Abstract:
In mitotic cells, cellular senescence is a permanent state of G1 arrest, that may have evolved in parallel to apoptosis, to limit proliferation of damaged cells and oncogenesis. Recent studies have suggested that postmitotic cells are also capable of entering a state of senescence, although the repercussions of postmitotic cellular senescence (PoMiCS) on tissue health and function are currently ill-defined. In tissues made largely of post-mitotic cells, it is evolutionary advantageous to preserve cellular integrity and cellular senescence of post-mitotic cells may prevent stressor-induced tissue degeneration and promote tissue repair. Paradoxically, PoMiCS may also contribute to disease progression through the generation of inflammatory mediators, termed the senescence-associated secretory phenotype. Here, we discuss the potential roles of PoMiCS and propose to enlarge the current definition of cellular senescence to postmitotic terminally differentiated cells.
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