Tracking the dynamics of cellular senescence
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Tracking the dynamics of cellular senescence. / Heckenbach, Indra; Scheibye-Knudsen, Morten.
In: Aging, Vol. 15, No. 9, 2023, p. 3219-3220.Research output: Contribution to journal › Editorial › Research › peer-review
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TY - JOUR
T1 - Tracking the dynamics of cellular senescence
AU - Heckenbach, Indra
AU - Scheibye-Knudsen, Morten
N1 - Publisher Copyright: © 2023 Heckenbach and Scheibye-Knudsen. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
PY - 2023
Y1 - 2023
N2 - Cellular senescence, often defined as a state of permanent cell cycle arrest, is a complex and multifaceted process that arises in diverse contexts. First identified as the end point of replicative exhaustion [1], senescence also arises from DNA damage, mitochondrial dysfunction, oxidative stress, sustained mitogenic signaling through oncogenes, proteostatic stress and other. Senescence is under normal physiological conditions involved in wound healing and embryogenesis. Diverse processes trigger multiple mechanisms that converge into cell cycle arrest and a secretory phenotype. Two key pathways may lead to senescence, including the stress-associated p16/Rb pathway and the p53/p21 damage control mechanism. Senescence has been further characterized by its inflammatory secretome (SASP) that serves to signal immune clearance, although it differs by cell type and method of senescence induction. Despite its variable secretome, the SASP may better define senescence since nondividing cells including neurons and cardiomyocytes may exhibit senescent characteristics, despite being frozen at the G0/G1 stage in the cell cycle
AB - Cellular senescence, often defined as a state of permanent cell cycle arrest, is a complex and multifaceted process that arises in diverse contexts. First identified as the end point of replicative exhaustion [1], senescence also arises from DNA damage, mitochondrial dysfunction, oxidative stress, sustained mitogenic signaling through oncogenes, proteostatic stress and other. Senescence is under normal physiological conditions involved in wound healing and embryogenesis. Diverse processes trigger multiple mechanisms that converge into cell cycle arrest and a secretory phenotype. Two key pathways may lead to senescence, including the stress-associated p16/Rb pathway and the p53/p21 damage control mechanism. Senescence has been further characterized by its inflammatory secretome (SASP) that serves to signal immune clearance, although it differs by cell type and method of senescence induction. Despite its variable secretome, the SASP may better define senescence since nondividing cells including neurons and cardiomyocytes may exhibit senescent characteristics, despite being frozen at the G0/G1 stage in the cell cycle
KW - aging
KW - cellular senescence
KW - deep learning
KW - nuclear morphology
KW - quantitative senescence
U2 - 10.18632/aging.204670
DO - 10.18632/aging.204670
M3 - Editorial
C2 - 37071012
AN - SCOPUS:85159775272
VL - 15
SP - 3219
EP - 3220
JO - Aging
JF - Aging
SN - 1945-4589
IS - 9
ER -
ID: 371282331