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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Published in:GeroScience Vol. 42; no. 2; pp. 397 - 408
Main Authors: Anerillas, Carlos, Abdelmohsen, Kotb, Gorospe, Myriam
Format: Journal Article
Language:English
Published: Cham Springer International Publishing 01.04.2020
Springer Nature B.V
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ISSN:2509-2715, 2509-2723, 2509-2723
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Abstract 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.
AbstractList 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.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.
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.
Author Anerillas, Carlos
Gorospe, Myriam
Abdelmohsen, Kotb
Author_xml – sequence: 1
  givenname: Carlos
  orcidid: 0000-0003-4424-7913
  surname: Anerillas
  fullname: Anerillas, Carlos
  organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health
– sequence: 2
  givenname: Kotb
  orcidid: 0000-0001-6240-5810
  surname: Abdelmohsen
  fullname: Abdelmohsen, Kotb
  organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health
– sequence: 3
  givenname: Myriam
  orcidid: 0000-0001-5439-3434
  surname: Gorospe
  fullname: Gorospe, Myriam
  email: myriam-gorospe@nih.gov
  organization: Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32300964$$D View this record in MEDLINE/PubMed
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Fri Feb 21 02:42:16 EST 2025
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Issue 2
Keywords Senescence
p38
Gene expression programs
SASP
JNK
ERK
Language English
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content type line 14
ObjectType-Review-3
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ORCID 0000-0001-6240-5810
0000-0001-5439-3434
0000-0003-4424-7913
OpenAccessLink https://link.springer.com/content/pdf/10.1007/s11357-020-00183-3.pdf
PMID 32300964
PQID 2399900102
PQPubID 326370
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crossref_primary_10_1007_s11357_020_00183_3
crossref_citationtrail_10_1007_s11357_020_00183_3
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PublicationCentury 2000
PublicationDate 2020-04-01
PublicationDateYYYYMMDD 2020-04-01
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  year: 2020
  text: 2020-04-01
  day: 01
PublicationDecade 2020
PublicationPlace Cham
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– name: Switzerland
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PublicationSubtitle Official Journal of the American Aging Association (AGE)
PublicationTitle GeroScience
PublicationTitleAbbrev GeroScience
PublicationTitleAlternate Geroscience
PublicationYear 2020
Publisher Springer International Publishing
Springer Nature B.V
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Snippet A phenotype of indefinite growth arrest acquired in response to sublethal damage, cellular senescence affects normal aging and age-related disease....
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SubjectTerms 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
Title Regulation of senescence traits by MAPKs
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