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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Bibliographic Details
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
Cellular Senescence
Humans
mitochondria
Mitochondria - pathology
Phenotype
senescence
senolytics
senostatics
senescence
senolytics
ageing
mitochondria
senostatics
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Summary: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.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
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ObjectType-Review-1
ISSN:0014-5793
1873-3468
DOI:10.1002/1873-3468.13498