Review
Version 1
Preserved in Portico This version is not peer-reviewed
Is “Cellular Senescence” a Misnomer?
Version 1
: Received: 26 July 2022 / Approved: 27 July 2022 / Online: 27 July 2022 (13:38:36 CEST)
How to cite: Gems, D.; Kern, C. Is “Cellular Senescence” a Misnomer?. Preprints 2022, 2022070423. https://doi.org/10.20944/preprints202207.0423.v1 Gems, D.; Kern, C. Is “Cellular Senescence” a Misnomer?. Preprints 2022, 2022070423. https://doi.org/10.20944/preprints202207.0423.v1
Abstract
One of the most striking findings in biogerontology in the 2010s was the demonstration that elimination of senescent cells delays many late-life diseases and extends lifespan in mice. This implied that accumulation of senescent cells promotes late-life diseases, particularly through action of senescent cell secretions (the senescence-associated secretory phenotype or SASP). But what exactly is a senescent cell? Subsequent to the initial characterization of cellular senescence it became clear that, prior to aging, this phenomenon is in fact adaptive. It supports tissue remodeling functions in a variety of contexts, including embryogenesis, parturition and acute inflammatory processes that restore normal tissue architecture and function, such as wound healing, tissue repair after infection, and amphibian limb regeneration. In these contexts such cells are normal and healthy, and not in any way senescent in the true sense of the word, as originally meant by Hayflick. Thus, it is misleading to refer to them as “senescent”. Similarly, the common assertion that senescent cells accumulate with age due to stress and DNA damage is no longer safe, particularly given their role in inflammation - a process that becomes persistent in later life. We therefore suggest that it would be useful to update some terminology, to bring it into line with contemporary understanding, and to avoid future confusion. To open a discussion of this issue, we propose replacing the term cellular senescence with remodeling activation, and SASP with RASP (remodeling-associated secretory phenotype).
Keywords
Aging; cellular senescence; fibroblast; osteoarthritis; remodeling-associated secretory phenotype (RASP); remodeling activation
Subject
Biology and Life Sciences, Cell and Developmental Biology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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