From cell senescence to age-related diseases: differential mechanisms of action of senescence-associated secretory phenotypes

Cellular senescence is a process by which cells enter a state of permanent cell cycle arrest. It is commonly believed to underlie organismal aging and age-associated diseases. However, the mechanism by which cellular senescence contributes to aging and age-associated pathologies remains unclear. Rec...

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Published inBMB reports Vol. 48; no. 10; pp. 549 - 558
Main Authors Byun, H.O., Ajou University, Suwon, Republic of Korea, Lee, Y.K., Ajou University, Suwon, Republic of Korea, Kim, J.M., Ajou University, Suwon, Republic of Korea, Yoon, G., Ajou University, Suwon, Republic of Korea
Format Journal Article
LanguageEnglish
Published Korea (South) Korean Society for Biochemistry and Molecular Biology 01.10.2015
생화학분자생물학회
Subjects
Age Factors
Age-associated diseases,Cell senescence,Differential expression, Senescence-associated secretory phenotypes (SASP)
Animals
Cellular Senescence - genetics
Cellular Senescence - physiology
FENOTIPOS
Humans
Invited Mini Review
PHENOTYPE
PHENOTYPES
Secretory Pathway - genetics
Secretory Pathway - physiology
화학
Online AccessGet full text
ISSN1976-6696
1976-670X
DOI10.5483/BMBRep.2015.48.10.122

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Abstract Cellular senescence is a process by which cells enter a state of permanent cell cycle arrest. It is commonly believed to underlie organismal aging and age-associated diseases. However, the mechanism by which cellular senescence contributes to aging and age-associated pathologies remains unclear. Recent studies showed that senescent cells exert detrimental effects on the tissue microenvironment, generating pathological facilitators or aggravators. The most significant environmental effector resulting from senescent cells is the senescence-associated secretory phenotype (SASP), which is constituted by a strikingly increased expression and secretion of diverse pro-inflammatory cytokines. Careful investigation into the components of SASPs and their mechanism of action, may improve our understanding of the pathological backgrounds of age-associated diseases. In this review, we focus on the differential expression of SASP-related genes, in addition to SASP components, during the progress of senescence. We also provide a perspective on the possible action mechanisms of SASP components, and potential contributions of SASP-expressing senescent cells, to age-associated pathologies.
AbstractList Cellular senescence is a process by which cells enter a state of permanent cell cycle arrest. It is commonly believed to underlie organismal aging and age-associated diseases. However, the mechanism by which cellular senescence contributes to aging and age-associated pathologies remains unclear. Recent studies showed that senescent cells exert detrimental effects on the tissue microenvironment, generating pathological facilitators or aggravators. The most significant environmental effector resulting from senescent cells is the senescence-associated secretory phenotype (SASP), which is constituted by a strikingly increased expression and secretion of diverse pro-inflammatory cytokines. Careful investigation into the components of SASPs and their mechanism of action, may improve our understanding of the pathological backgrounds of age-associated diseases. In this review, we focus on the differential expression of SASP-related genes, in addition to SASP components, during the progress of senescence. We also provide a perspective on the possible action mechanisms of SASP components, and potential contributions of SASP-expressing senescent cells, to age-associated pathologies. KCI Citation Count: 18
Cellular senescence is a process by which cells enter a state of permanent cell cycle arrest. It is commonly believed to underlie organismal aging and age-associated diseases. However, the mechanism by which cellular senescence contributes to aging and age-associated pathologies remains unclear. Recent studies showed that senescent cells exert detrimental effects on the tissue microenvironment, generating pathological facilitators or aggravators. The most significant environmental effector resulting from senescent cells is the senescence-associated secretory phenotype (SASP), which is constituted by a strikingly increased expression and secretion of diverse pro-inflammatory cytokines. Careful investigation into the components of SASPs and their mechanism of action, may improve our understanding of the pathological backgrounds of age-associated diseases. In this review, we focus on the differential expression of SASP-related genes, in addition to SASP components, during the progress of senescence. We also provide a perspective on the possible action mechanisms of SASP components, and potential contributions of SASP-expressing senescent cells, to age-associated pathologies.
Cellular senescence is a process by which cells enter a state of permanent cell cycle arrest. It is commonly believed to underlie organismal aging and age-associated diseases. However, the mechanism by which cellular senescence contributes to aging and age-associated pathologies remains unclear. Recent studies showed that senescent cells exert detrimental effects on the tissue microenvironment, generating pathological facilitators or aggravators. The most significant environmental effector resulting from senescent cells is the senescence-associated secretory phenotype (SASP), which is constituted by a strikingly increased expression and secretion of diverse pro-inflammatory cytokines. Careful investigation into the components of SASPs and their mechanism of action, may improve our understanding of the pathological backgrounds of age-associated diseases. In this review, we focus on the differential expression of SASP-related genes, in addition to SASP components, during the progress of senescence. We also provide a perspective on the possible action mechanisms of SASP components, and potential contributions of SASP-expressing senescent cells, to age-associated pathologies. [BMB Reports 2015; 48(10): 549-558]
Author Byun, H.O., Ajou University, Suwon, Republic of Korea
Lee, Y.K., Ajou University, Suwon, Republic of Korea
Yoon, G., Ajou University, Suwon, Republic of Korea
Kim, J.M., Ajou University, Suwon, Republic of Korea
AuthorAffiliation 1 Department of Biochemistry, Ajou University School of Medicine
2 Department of Biomedical Science, Graduate School
3 College of Natural Sciences, Ajou University, Suwon 16499, Korea
AuthorAffiliation_xml – name: 1 Department of Biochemistry, Ajou University School of Medicine
– name: 2 Department of Biomedical Science, Graduate School
– name: 3 College of Natural Sciences, Ajou University, Suwon 16499, Korea
Author_xml – sequence: 1
  fullname: Byun, H.O., Ajou University, Suwon, Republic of Korea
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  fullname: Lee, Y.K., Ajou University, Suwon, Republic of Korea
– sequence: 3
  fullname: Kim, J.M., Ajou University, Suwon, Republic of Korea
– sequence: 4
  fullname: Yoon, G., Ajou University, Suwon, Republic of Korea
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Snippet Cellular senescence is a process by which cells enter a state of permanent cell cycle arrest. It is commonly believed to underlie organismal aging and...
SourceID nrf
pubmedcentral
pubmed
crossref
fao
SourceType Open Website
Open Access Repository
Index Database
Enrichment Source
Publisher
StartPage 549
SubjectTerms Age Factors
Age-associated diseases,Cell senescence,Differential expression, Senescence-associated secretory phenotypes (SASP)
Animals
Cellular Senescence - genetics
Cellular Senescence - physiology
FENOTIPOS
Humans
Invited Mini Review
PHENOTYPE
PHENOTYPES
Secretory Pathway - genetics
Secretory Pathway - physiology
화학
Title From cell senescence to age-related diseases: differential mechanisms of action of senescence-associated secretory phenotypes
URI https://www.ncbi.nlm.nih.gov/pubmed/26129674
https://pubmed.ncbi.nlm.nih.gov/PMC4911181
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Volume 48
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