Mitochondrial dysfunction and cell senescence: deciphering a complex relationship

Cellular senescence and mitochondrial dysfunction have both been defined as classical hallmarks of the ageing process. Here, we review the intricate relationship between the two. In the context of ageing, it is now well regarded that cellular senescence is a key driver in both ageing and the onset o...

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Published inFEBS letters Vol. 593; no. 13; pp. 1566 - 1579
Main Authors Chapman, James, Fielder, Edward, Passos, João F.
Format Journal Article
LanguageEnglish
Published England 01.07.2019
Subjects
ageing
Aging - pathology
Animals
cell senescence
Cellular Senescence
Humans
metabolites
mitochondria
Mitochondria - pathology
Phenotype
reactive oxygen species
senescence
senolytics
senostatics
therapeutics
senescence
senolytics
ageing
mitochondria
senostatics
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Abstract Cellular senescence and mitochondrial dysfunction have both been defined as classical hallmarks of the ageing process. Here, we review the intricate relationship between the two. In the context of ageing, it is now well regarded that cellular senescence is a key driver in both ageing and the onset of a number of age‐related pathologies. Emerging evidence has pinpointed mitochondria as one of the key modulators in the development of the senescence phenotype, particularly the pro‐inflammatory senescence associated secretory phenotype (SASP). This review focuses on the contribution of homeostatic mechanisms, as well as of reactive oxygen species and mitochondrial metabolites in the senescence programme. Furthermore, we discuss emerging pathways and mitochondrial‐mediated mechanisms that may be influencing the SASP and, subsequently, explore how these may be exploited to open up new therapeutic avenues.
AbstractList Cellular senescence and mitochondrial dysfunction have both been defined as classical hallmarks of the ageing process. Here, we review the intricate relationship between the two. In the context of ageing, it is now well regarded that cellular senescence is a key driver in both ageing and the onset of a number of age‐related pathologies. Emerging evidence has pinpointed mitochondria as one of the key modulators in the development of the senescence phenotype, particularly the pro‐inflammatory senescence associated secretory phenotype (SASP). This review focuses on the contribution of homeostatic mechanisms, as well as of reactive oxygen species and mitochondrial metabolites in the senescence programme. Furthermore, we discuss emerging pathways and mitochondrial‐mediated mechanisms that may be influencing the SASP and, subsequently, explore how these may be exploited to open up new therapeutic avenues.
Cellular senescence and mitochondrial dysfunction have both been defined as classical hallmarks of the ageing process. Here, we review the intricate relationship between the two. In the context of ageing, it is now well regarded that cellular senescence is a key driver in both ageing and the onset of a number of age-related pathologies. Emerging evidence has pinpointed mitochondria as one of the key modulators in the development of the senescence phenotype, particularly the pro-inflammatory senescence associated secretory phenotype (SASP). This review focuses on the contribution of homeostatic mechanisms, as well as of reactive oxygen species and mitochondrial metabolites in the senescence programme. Furthermore, we discuss emerging pathways and mitochondrial-mediated mechanisms that may be influencing the SASP and, subsequently, explore how these may be exploited to open up new therapeutic avenues.Cellular senescence and mitochondrial dysfunction have both been defined as classical hallmarks of the ageing process. Here, we review the intricate relationship between the two. In the context of ageing, it is now well regarded that cellular senescence is a key driver in both ageing and the onset of a number of age-related pathologies. Emerging evidence has pinpointed mitochondria as one of the key modulators in the development of the senescence phenotype, particularly the pro-inflammatory senescence associated secretory phenotype (SASP). This review focuses on the contribution of homeostatic mechanisms, as well as of reactive oxygen species and mitochondrial metabolites in the senescence programme. Furthermore, we discuss emerging pathways and mitochondrial-mediated mechanisms that may be influencing the SASP and, subsequently, explore how these may be exploited to open up new therapeutic avenues.
Author Chapman, James
Passos, João F.
Fielder, Edward
Author_xml – sequence: 1
  givenname: James
  surname: Chapman
  fullname: Chapman, James
  organization: Newcastle University Institute for Ageing, Newcastle University
– sequence: 2
  givenname: Edward
  surname: Fielder
  fullname: Fielder, Edward
  organization: Newcastle University Institute for Ageing, Newcastle University
– sequence: 3
  givenname: João F.
  surname: Passos
  fullname: Passos, João F.
  email: passos.joao@mayo.edu
  organization: Mayo Clinic
BackLink https://www.ncbi.nlm.nih.gov/pubmed/31211858$$D View this record in MEDLINE/PubMed
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ISSN 0014-5793
1873-3468
IngestDate Fri Jul 11 18:23:48 EDT 2025
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Mon Jul 21 06:02:54 EDT 2025
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Issue 13
Keywords senescence
senolytics
ageing
mitochondria
senostatics
Language English
License 2019 Federation of European Biochemical Societies.
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SecondaryResourceType review_article
Snippet Cellular senescence and mitochondrial dysfunction have both been defined as classical hallmarks of the ageing process. Here, we review the intricate...
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StartPage 1566
SubjectTerms ageing
Aging - pathology
Animals
cell senescence
Cellular Senescence
Humans
metabolites
mitochondria
Mitochondria - pathology
Phenotype
reactive oxygen species
senescence
senolytics
senostatics
therapeutics
Title Mitochondrial dysfunction and cell senescence: deciphering a complex relationship
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2F1873-3468.13498
https://www.ncbi.nlm.nih.gov/pubmed/31211858
https://www.proquest.com/docview/2243490979
https://www.proquest.com/docview/2718339093
Volume 593
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