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 -