Non-Intrinsic, Systemic Mechanisms of Cellular Senescence

Cellular senescence is believed to contribute to aging and disease through the activity of secreted factors that promote inflammation, remodel the extracellular matrix, and adversely modify the behavior of non-senescent cells. While the markers and properties of senescent cells are still under inves...

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Main Authors: Rachael E. Schwartz, Irina M. Conboy
Format: Article
Language:English
Published: MDPI AG 2023-12-01
Series:Cells
Subjects:
Online Access:https://www.mdpi.com/2073-4409/12/24/2769
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author Rachael E. Schwartz
Irina M. Conboy
author_facet Rachael E. Schwartz
Irina M. Conboy
author_sort Rachael E. Schwartz
collection DOAJ
description Cellular senescence is believed to contribute to aging and disease through the activity of secreted factors that promote inflammation, remodel the extracellular matrix, and adversely modify the behavior of non-senescent cells. While the markers and properties of senescent cells are still under investigation, it is postulated that cellular senescence manifests in vivo as the consequence of cellular damage that accumulates and becomes exacerbated with time. Yet, the notions that senescence has a solely intrinsic and time-dependent nature are questioned by the rapid induction of senescence in young mice and young cells in vitro by exposure to blood from aged animals. Here, we review some of the research on the systemically present factors that increase with age and may contribute to extrinsically induced senescence or “bystander senescence”. These include proteins, reactive oxygen species, lipids, and nucleic acids, which may be present in individual soluble form, in vesicles, and in non-membranous multi-component macromolecules.
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spelling doaj.art-ed32d06170e74e58a7c5681a36a8e6492023-12-22T13:59:31ZengMDPI AGCells2073-44092023-12-011224276910.3390/cells12242769Non-Intrinsic, Systemic Mechanisms of Cellular SenescenceRachael E. Schwartz0Irina M. Conboy1Department of Bioengineering, University of California Berkeley, Berkeley, CA 94720, USADepartment of Bioengineering, University of California Berkeley, Berkeley, CA 94720, USACellular senescence is believed to contribute to aging and disease through the activity of secreted factors that promote inflammation, remodel the extracellular matrix, and adversely modify the behavior of non-senescent cells. While the markers and properties of senescent cells are still under investigation, it is postulated that cellular senescence manifests in vivo as the consequence of cellular damage that accumulates and becomes exacerbated with time. Yet, the notions that senescence has a solely intrinsic and time-dependent nature are questioned by the rapid induction of senescence in young mice and young cells in vitro by exposure to blood from aged animals. Here, we review some of the research on the systemically present factors that increase with age and may contribute to extrinsically induced senescence or “bystander senescence”. These include proteins, reactive oxygen species, lipids, and nucleic acids, which may be present in individual soluble form, in vesicles, and in non-membranous multi-component macromolecules.https://www.mdpi.com/2073-4409/12/24/2769agingcellular senescencebystander senescencesystemic milieublood serum and plasma
spellingShingle Rachael E. Schwartz
Irina M. Conboy
Non-Intrinsic, Systemic Mechanisms of Cellular Senescence
Cells
aging
cellular senescence
bystander senescence
systemic milieu
blood serum and plasma
title Non-Intrinsic, Systemic Mechanisms of Cellular Senescence
title_full Non-Intrinsic, Systemic Mechanisms of Cellular Senescence
title_fullStr Non-Intrinsic, Systemic Mechanisms of Cellular Senescence
title_full_unstemmed Non-Intrinsic, Systemic Mechanisms of Cellular Senescence
title_short Non-Intrinsic, Systemic Mechanisms of Cellular Senescence
title_sort non intrinsic systemic mechanisms of cellular senescence
topic aging
cellular senescence
bystander senescence
systemic milieu
blood serum and plasma
url https://www.mdpi.com/2073-4409/12/24/2769
work_keys_str_mv AT rachaeleschwartz nonintrinsicsystemicmechanismsofcellularsenescence
AT irinamconboy nonintrinsicsystemicmechanismsofcellularsenescence