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Lookup NU author(s): Professor Thomas von Zglinicki,
Dr Tengfei Wan,
Dr Satomi Miwa
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
© Thomas von Zglinicki et al. 2021; Published by Mary Ann Liebert, Inc.Significance: Cell senescence was originally defined by an acute loss of replicative capacity and thus believed to be restricted to proliferation-competent cells. More recently, senescence has been recognized as a cellular stress and damage response encompassing multiple pathways or senescence domains, namely DNA damage response, cell cycle arrest, senescence-associated secretory phenotype, senescence-associated mitochondrial dysfunction, autophagy/mitophagy dysfunction, nutrient and stress signaling, and epigenetic reprogramming. Each of these domains is activated during senescence, and all appear to interact with each other. Cell senescence has been identified as an important driver of mammalian aging. Recent Advances: Activation of all these senescence domains has now also been observed in a wide range of post-mitotic cells, suggesting that senescence as a stress response can occur in nondividing cells temporally uncoupled from cell cycle arrest. Here, we review recent evidence for post-mitotic cell senescence and speculate about its possible relevance for mammalian aging. Critical Issues: Although a majority of senescence domains has been found to be activated in a range of post-mitotic cells during aging, independent confirmation of these results is still lacking for most of them. Future Directions: To define whether post-mitotic senescence plays a significant role as a driver of aging phenotypes in tissues such as brain, muscle, heart, and others. Antioxid. Redox Signal. 34, 308-323.
Author(s): Von Zglinicki T, Wan T, Miwa S
Publication type: Review
Publication status: Published
Journal: Antioxidants and Redox Signaling
Print publication date: 01/02/2021
Online publication date: 27/04/2021
Acceptance date: 09/03/2020
ISSN (print): 1523-0864
ISSN (electronic): 1557-7716
Publisher: Mary Ann Liebert Inc.
PubMed id: 32164429