Cellular senescence: all roads lead to mitochondria

Senescence is a multi‐functional cell fate, characterized by an irreversible cell‐cycle arrest and a pro‐inflammatory phenotype, commonly known as the senescence‐associated secretory phenotype (SASP). Emerging evidence indicates that accumulation of senescent cells in multiple tissues drives tissue...

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Published inThe FEBS journal Vol. 290; no. 5; pp. 1186 - 1202
Main Authors Martini, Hélène, Passos, João F.
Format Journal Article
LanguageEnglish
Published England Blackwell Publishing Ltd 01.03.2023
Subjects
ageing
cell cycle checkpoints
Cell death
Cell fate
cell senescence
Cellular Senescence
industry
Inflammation
Mitochondria
Phenotype
Phenotypes
SASP
Senescence
Therapeutic applications
therapeutics
senescence
ageing
SASP
mitochondria
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Abstract Senescence is a multi‐functional cell fate, characterized by an irreversible cell‐cycle arrest and a pro‐inflammatory phenotype, commonly known as the senescence‐associated secretory phenotype (SASP). Emerging evidence indicates that accumulation of senescent cells in multiple tissues drives tissue dysfunction and several age‐related conditions. This has spurred the academic community and industry to identify new therapeutic interventions targeting this process. Mitochondrial dysfunction is an often‐unappreciated hallmark of cellular senescence which plays important roles not only in the senescence growth arrest but also in the development of the SASP and resistance to cell‐death. Here, we review the evidence that supports a role for mitochondria in the development of senescence and describe the underlying mechanisms. Finally, we propose that a detailed road map of mitochondrial biology in senescence will be crucial to guide the future development of senotherapies. Mitochondria play a central role in the development of cellular senescence. Senescence is characterized by several mitochondrial functional changes such as a decrease in OXPHOS, reduced levels of NAD+ and ATP, and accumulation of TCA cycle metabolites, DAMPs, and ROS. Here, we provide an overview of the recent findings demonstrating how these mitochondrial changes can contribute to the senescence‐associated growth arrest and the SASP.
AbstractList Senescence is a multi-functional cell fate, characterized by an irreversible cell-cycle arrest and a pro-inflammatory phenotype, commonly known as the senescence-associated secretory phenotype (SASP). Emerging evidence indicates that accumulation of senescent cells in multiple tissues drives tissue dysfunction and several age-related conditions. This has spurred the academic community and industry to identify new therapeutic interventions targeting this process. Mitochondrial dysfunction is an often-unappreciated hallmark of cellular senescence which plays important roles not only in the senescence growth arrest but also in the development of the SASP and resistance to cell-death. Here, we review the evidence that supports a role for mitochondria in the development of senescence and describe the underlying mechanisms. Finally, we propose that a detailed road map of mitochondrial biology in senescence will be crucial to guide the future development of senotherapies.
Senescence is a multi-functional cell fate, characterized by an irreversible cell-cycle arrest and a pro-inflammatory phenotype, commonly known as the Senescence-Associated secretory Phenotype (SASP). Emerging evidence indicates that accumulation of senescent cells in multiple tissues, drives tissue dysfunction and several age-related conditions. This has spurred the academic community and industry to identify new therapeutic interventions targeting this process. Mitochondrial dysfunction is an often-unappreciated hallmark of cellular senescence which plays important roles not only in the senescence growth arrest but also in the development of the SASP and resistance to cell-death. Here, we review the evidence that supports a role for mitochondria in the development of senescence and describe the underlying mechanisms. Finally, we propose that a detailed road map of mitochondrial biology in senescence will be crucial to guide the future development of senotherapies. Mitochondria play a central role in the development of cellular senescence. Senescence is characterized by several mitochondrial functional changes such as a decrease in OXPHOS, reduced levels of NAD+ and ATP and accumulation of TCA cycle metabolites, DAMPs, and ROS. Here, we provide an overview of the recent findings demonstrating how these mitochondrial changes can contribute to the senescence-associated growth arrest and the SASP.
Senescence is a multi-functional cell fate, characterized by an irreversible cell-cycle arrest and a pro-inflammatory phenotype, commonly known as the senescence-associated secretory phenotype (SASP). Emerging evidence indicates that accumulation of senescent cells in multiple tissues drives tissue dysfunction and several age-related conditions. This has spurred the academic community and industry to identify new therapeutic interventions targeting this process. Mitochondrial dysfunction is an often-unappreciated hallmark of cellular senescence which plays important roles not only in the senescence growth arrest but also in the development of the SASP and resistance to cell-death. Here, we review the evidence that supports a role for mitochondria in the development of senescence and describe the underlying mechanisms. Finally, we propose that a detailed road map of mitochondrial biology in senescence will be crucial to guide the future development of senotherapies.Senescence is a multi-functional cell fate, characterized by an irreversible cell-cycle arrest and a pro-inflammatory phenotype, commonly known as the senescence-associated secretory phenotype (SASP). Emerging evidence indicates that accumulation of senescent cells in multiple tissues drives tissue dysfunction and several age-related conditions. This has spurred the academic community and industry to identify new therapeutic interventions targeting this process. Mitochondrial dysfunction is an often-unappreciated hallmark of cellular senescence which plays important roles not only in the senescence growth arrest but also in the development of the SASP and resistance to cell-death. Here, we review the evidence that supports a role for mitochondria in the development of senescence and describe the underlying mechanisms. Finally, we propose that a detailed road map of mitochondrial biology in senescence will be crucial to guide the future development of senotherapies.
Senescence is a multi‐functional cell fate, characterized by an irreversible cell‐cycle arrest and a pro‐inflammatory phenotype, commonly known as the senescence‐associated secretory phenotype (SASP). Emerging evidence indicates that accumulation of senescent cells in multiple tissues drives tissue dysfunction and several age‐related conditions. This has spurred the academic community and industry to identify new therapeutic interventions targeting this process. Mitochondrial dysfunction is an often‐unappreciated hallmark of cellular senescence which plays important roles not only in the senescence growth arrest but also in the development of the SASP and resistance to cell‐death. Here, we review the evidence that supports a role for mitochondria in the development of senescence and describe the underlying mechanisms. Finally, we propose that a detailed road map of mitochondrial biology in senescence will be crucial to guide the future development of senotherapies. Mitochondria play a central role in the development of cellular senescence. Senescence is characterized by several mitochondrial functional changes such as a decrease in OXPHOS, reduced levels of NAD+ and ATP, and accumulation of TCA cycle metabolites, DAMPs, and ROS. Here, we provide an overview of the recent findings demonstrating how these mitochondrial changes can contribute to the senescence‐associated growth arrest and the SASP.
Author Passos, João F.
Martini, Hélène
AuthorAffiliation 1 Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, 55905 USA
2 Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, 55905 USA
AuthorAffiliation_xml – name: 1 Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, 55905 USA
– name: 2 Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, 55905 USA
Author_xml – sequence: 1
  givenname: Hélène
  surname: Martini
  fullname: Martini, Hélène
  organization: Mayo Clinic
– sequence: 2
  givenname: João F.
  orcidid: 0000-0001-8765-1890
  surname: Passos
  fullname: Passos, João F.
  email: passos.joao@mayo.edu
  organization: Mayo Clinic
BackLink https://www.ncbi.nlm.nih.gov/pubmed/35048548$$D View this record in MEDLINE/PubMed
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IngestDate Thu Aug 21 18:35:23 EDT 2025
Fri Jul 11 18:26:22 EDT 2025
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Issue 5
Keywords senescence
ageing
SASP
mitochondria
Language English
License 2022 Federation of European Biochemical Societies.
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content type line 14
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Author contributions: HM and JFP wrote the manuscript, HM created the figures and graphical abstract.
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Snippet Senescence is a multi‐functional cell fate, characterized by an irreversible cell‐cycle arrest and a pro‐inflammatory phenotype, commonly known as the...
Senescence is a multi-functional cell fate, characterized by an irreversible cell-cycle arrest and a pro-inflammatory phenotype, commonly known as the...
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SubjectTerms ageing
cell cycle checkpoints
Cell death
Cell fate
cell senescence
Cellular Senescence
industry
Inflammation
Mitochondria
Phenotype
Phenotypes
SASP
Senescence
Therapeutic applications
therapeutics
Title Cellular senescence: all roads lead to mitochondria
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Ffebs.16361
https://www.ncbi.nlm.nih.gov/pubmed/35048548
https://www.proquest.com/docview/2780744600
https://www.proquest.com/docview/2621661276
https://www.proquest.com/docview/2811979615
https://pubmed.ncbi.nlm.nih.gov/PMC9296701
Volume 290
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