Regulation of senescence traits by MAPKs

A phenotype of indefinite growth arrest acquired in response to sublethal damage, cellular senescence affects normal aging and age-related disease. Mitogen-activated protein kinases (MAPKs) are capable of sensing changes in cellular conditions, and in turn elicit adaptive responses including cell se...

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Vydané v:GeroScience Ročník 42; číslo 2; s. 397 - 408
Hlavní autori: Anerillas, Carlos, Abdelmohsen, Kotb, Gorospe, Myriam
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Cham Springer International Publishing 01.04.2020
Springer Nature B.V
Predmet:
Age differences
Aging
Arrests
Biomedical and Life Sciences
Cell Biology
Cell survival
Cellular Senescence
Elimination
Exploitation
Geriatrics/Gerontology
Inflammation
Kinases
Life Sciences
Mitogen-Activated Protein Kinases
Molecular Medicine
p38 Mitogen-Activated Protein Kinases - metabolism
p53 Protein
Phenotype
Phenotypes
Proteins
Reference (Semantic)
Review
Senescence
Signal Transduction
Senescence
p38
Gene expression programs
SASP
JNK
ERK
ISSN:2509-2715, 2509-2723, 2509-2723
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Popis
Shrnutí:A phenotype of indefinite growth arrest acquired in response to sublethal damage, cellular senescence affects normal aging and age-related disease. Mitogen-activated protein kinases (MAPKs) are capable of sensing changes in cellular conditions, and in turn elicit adaptive responses including cell senescence. MAPKs modulate the levels and function of many proteins, including proinflammatory factors and factors in the p21/p53 and p16/RB pathways, the main senescence-regulatory axes. Through these actions, MAPKs implement key traits of senescence—growth arrest, cell survival, and the senescence-associated secretory phenotype (SASP). In this review, we summarize and discuss our current knowledge of the impact of MAPKs in senescence. In addition, given that eliminating or suppressing senescent cells can improve health span, we discuss the function and possible exploitation of MAPKs in the elimination (senolysis) or suppression (senostasis) of senescent cells.
Bibliografia:ObjectType-Article-1
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ISSN:2509-2715
2509-2723
2509-2723
DOI:10.1007/s11357-020-00183-3