Regulation of Survival Networks in Senescent Cells: From Mechanisms to Interventions

Abel Soto-Gamez, Wim J. Quax, Marco Demaria*

*Corresponding author for this work

Research output: Contribution to journalReview articleAcademicpeer-review

61 Citations (Scopus)
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Cellular senescence is a state of stable cell cycle arrest arising in response to DNA and mitochondrial damages. Senescent cells undergo morphological, structural and functional changes that are influenced by a number of variables, including time, stress, tissue, and cell type. The heterogeneity of the senescent phenotype is exemplified by the many biological properties that senescent cells can cover. The advent of innovative model organisms has demonstrated a functional role of senescent cells during embryogenesis, tissue remodeling, tumorigenesis and aging. Importantly, prolonged and aberrant persistence of senescent cells is often associated with tissue dysfunction and pathology, and is partially the consequence of mechanisms that enhance survival and resistance to cell death. Here, we describe the main molecular players involved in promoting survival of senescent cells, with particular emphasis on the regulation of senescence-associated anti-apoptotic pathways. We discuss the consequences these pathways have in providing resistance to intrinsic and extrinsic pro-apoptotic signals. Finally, we highlight the importance of these pathways in the development of targets for senolytic interventions. (C) 2019 The Author(s). Published by Elsevier Ltd.

Original languageEnglish
Pages (from-to)2629-2643
Number of pages15
JournalJournal of Molecular Biology
Issue number15
Early online date31-May-2019
Publication statusPublished - 12-Jul-2019


  • aging
  • apoptosis
  • cell death
  • cellular senescence
  • cancer survival
  • carcinogenesis
  • cell aging
  • embryo development
  • human
  • review

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