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Cellular senescence and developmental defects
被引:4
|作者:
Klein, Annabelle
[1
,2
,3
,4
]
Rhinn, Muriel
[1
,2
,3
,4
]
Keyes, William M.
[1
,2
,3
,4
,5
]
机构:
[1] Inst Genet & Biol Mol & Cellulaire IGBMC, Illkirch Graffenstaden, France
[2] Ctr Natl Rech Sci CNRS, UMR7104, Illkirch Graffenstaden, France
[3] Inst Natl St & Rech Medicale INSERM, U1258, Illkirch Graffenstaden, France
[4] Univ Strasbourg, Illkirch Graffenstaden, France
[5] IGBMC, 1 Rue Laurent Fries,BP 10142, F-67404 Illkirch Graffenstaden, France
关键词:
developmental defect;
diabetes;
Down syndrome;
embryo;
neural tube defect;
neuroepithelial cell;
senescence;
senolytics;
valproic acid;
MOUSE MODEL;
CELLS;
P53;
GROWTH;
ACTIVATION;
EXPRESSION;
CLEARANCE;
MUTATIONS;
EXPOSURE;
DISRUPTS;
D O I:
10.1111/febs.16731
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Cellular senescence is a distinct state that is frequently induced in response to ageing and stress. Yet studies have also uncovered beneficial functions in development, repair and regeneration. Current opinion therefore suggests that timely and controlled induction of senescence can be beneficial, while misregulation of the senescence program, either through mis-timed activation, or chronic accumulation of senescent cells, contributes to many disease states and the ageing process. Whether atypical activation of senescence plays a role in the pathogenesis of developmental defects has been relatively underexplored. Here, we discuss three recent studies that implicate ectopic senescence in neurodevelopmental defects, with possible causative roles for senescence in these birth defects. In addition, we highlight how the examination of senescence in other birth defects is warranted, and speculate that aberrantly activated senescence may play a much broader role in developmental defects than currently appreciated.
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页码:1303 / 1313
页数:11
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