2016
DOI: 10.15252/embj.201592862
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Abstract: Cell senescence is an important tumour suppressor mechanism and driver of ageing. Both functions are dependent on the development of the senescent phenotype, which involves an overproduction of pro‐inflammatory and pro‐oxidant signals. However, the exact mechanisms regulating these phenotypes remain poorly understood. Here, we show the critical role of mitochondria in cellular senescence. In multiple models of senescence, absence of mitochondria reduced a spectrum of senescence effectors and phenotypes while p… Show more

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Cited by 535 publications
(538 citation statements)
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“…Mitochondrial dysfunction is obligatory for SASP production and cellular senescence (Correia‐Melo et al, 2016; Hutter et al, 2004). To examine mitochondrial bioenergetics, we performed high‐resolution respirometry to yield accurate quantitative measurements of oxidative phosphorylation in response to specific substrates for complex I, complex II, fat oxidation, and electron‐transfer system (ETS) capacity.…”
Section: Resultsmentioning
confidence: 99%
“…Mitochondrial dysfunction is obligatory for SASP production and cellular senescence (Correia‐Melo et al, 2016; Hutter et al, 2004). To examine mitochondrial bioenergetics, we performed high‐resolution respirometry to yield accurate quantitative measurements of oxidative phosphorylation in response to specific substrates for complex I, complex II, fat oxidation, and electron‐transfer system (ETS) capacity.…”
Section: Resultsmentioning
confidence: 99%
“…The mitochondrial mass increased following Tyr stimulation, as shown by the mitochondrial DNA copy number using mitoCytb and mitoNd1 (Figure 3a). Since previous studies have shown that increased mitochondrial biogenesis was part of the senescent phenotype, we measured the expression levels of its main transcriptional co‐activators, PGC‐1α and PGC‐1β (Correia‐Melo et al, 2016). mRNA analysis showed that PGC‐1β expression was increased with Tyr, while PGC‐1α was unchanged (Figure 3b).…”
Section: Resultsmentioning
confidence: 99%
“…Thus, mitochondrial dysfunction through ROS accumulation likely contributes to DDR establishment and senescence. In a previous study, Correia‐Melo et al (2016) reported that mitochondria were necessary for replicative and irradiation‐induced premature senescence in fibroblasts. In this case, they also observed mitochondrial ROS accumulation and increased mitochondrial mass, but the main drivers of senescence were mitochondrial biogenesis and PGC‐1β activation.…”
Section: Discussionmentioning
confidence: 98%
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