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Mitochondria are required for pro-ageing features of the senescent phenotype
Open accessAbstract
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 preserving ATP production via enhanced glycolysis. Global transcriptomic analysis by RNA sequencing revealed that a vast number of senescent‐associated changes are dependent on mitochondria, particularly the pro‐inflammatory phenotype. Mechanistically, we show that the ATM, Akt and mTORC1 phosphorylation cascade integrates signals from the DNA damage response (DDR) towards PGC‐1β‐dependent mitochondrial biogenesis, contributing to a ROS‐mediated activation of the DDR and cell cycle arrest. Finally, we demonstrate that the reduction in mitochondrial content in vivo , by either mTORC1 inhibition or PGC‐1β deletion, prevents senescence in the ageing mouse liver. Our results suggest that mitochondria are a candidate target for interventions to reduce the deleterious impact of senescence in ageing tissues.
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“There is evidence in support of a reciprocal influence between nuclear DNA damage and mitochondrial dysfunction48”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [48]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Targeting aspects of mitochondrial biology, such as the electron transport chain (ETC), complex I assembly, mitochondrial fission rates, and biogenesis, mitochondrial sirtuins and/or disruption of the TCA cycle can trigger senescence (Correia-Melo et al., 2016; Jiang et al., 2013; Kaplon et al., 2013; Miwa et al., 2014; Moiseeva et al., 2009; Park et al., 2010; Wiley et al., 2016).”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as Correia-Melo et al., 2016
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Mitochondrial dysfunction during senescence can result in ROS-driven lipid damage, lipid deposits (Correia-Melo et al., 2016; Ogrodnik et al., 2017), and lipofuscin accumulation (Gorgoulis et al., 2018).”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as Correia-Melo et al., 2016
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Mitochondrial dysfunction has been described as both a driver and consequence of cellular senescence”
From Length-independent telomere damage drives post-mitotic cardiomyocyte senescence (2019) · cites this paper as Correia‐Melo et al, 2016
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In the citing paper
“First, interventions known to increase health span such as dietary restriction41, exercise42, rapamycin43,44 and 17β-oestradiol45 can reduce the frequency of cells with TAFs.”
From Telomere dysfunction in ageing and age-related diseases (2022) · cites this paper as [43]
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In the citing paper
“Mitophagy (mitochondrial clearance) in senescent cells appears to suppress the SASP (Correia-Melo et al., 2016).”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as Correia-Melo et al., 2016
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In the citing paper
“Furthermore, dysfunctional mitochondria,195 persistent DNA damage response,196 CCAAT/enhancer-binding protein β (C/EBPβ) and NF-κB,197 mTOR, and other factors are involved in regulating SASP.194”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [195]
In the citing paper
“Altered mitochondrial function appears essential in mediating the senescence phenotype.”
From Ageing, Cellular Senescence and Neurodegenerative Disease (2018) · cites this paper as [60]
In the citing paper
“Many cells undergo senescence independently of telomere shorting due to replicative, mitochondrial, oxidative, metabolic, or genotoxic stress (Parrinello et al., 2003; Christoffersen et al., 2010; Correia-Melo et al., 2016; Nair et al., 2015).”
From DNA damage-how and why we age? (2021) · cites this paper as Correia-Melo et al., 2016
In the citing paper
“We have shown that a DNA damage response can induce mitochondrial ROS and this is partially dependent on the activation of p53 and p21 pathways, but also signals from ATM towards mTORC1 (Passos et al., 2010, Correia-Melo et al., 2016).”
From Telomeres and cell senescence—size matters not (2017) · cites this paper as Correia-Melo et al., 2016
In the citing paper
“Interestingly, mitochondrial ablation from senescent cells, or inhibition of mtROS formation, inhibits the SASP and prevents the formation of CCF, suggesting that mito-nuclear communication plays a role in CCF formation (Correia-Melo et al., 2016; Vizioli et al., 2020).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Correia-Melo et al., 2016
In the citing paper
“For instance, inhibition of the mTOR pathway (using the drug rapamycin), which has been shown to extend lifespan in a variety of model organisms (de Magalhaes et al., 2012;Harrison et al., 2009), is an effective SASP suppressor (Correia-Melo et al., 2016;Herranz et al., 2015;Laberge et al., 2015).”
From Stress, cell senescence and organismal ageing (2018) · cites this paper as Correia-Melo et al., 2016
In the citing paper
“Removal of mitochondria in senescent cells disrupts the feedforward cycle that involves ROS production and persistent DDR activation, while preserving their cell cycle arrest [215].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [215]
In the citing paper
“Similarly, during senescence, mTORC1 activation due to sustained DDR does not favor growth but promotes mitochondrial biogenesis, thus contributing to the ROS-dependent DDR persistence and to SASP regulation [215].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [215]
In the citing paper
“The switch from transient to irreversible growth arrest involves positive feedback loops in which mitochondrial dysfunction via ROS [215,250], pro-inflammatory SASP factors [147,154,252], extensive chromatin remodeling [253], and/or nuclear lamina and chromatin degradation [105,171,247] reinforce DDR signaling (Figure 3).”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [215]
In the citing paper
“The escalating ROS production by dysfunctional mitochondria aggravates nuclear DNA damage and stabilizes the chronic DDR activation, contributing to the maintenance of the pro-inflammatory and pro-oxidant senescent phenotype upon DNA damage [215,250].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [215]
In the citing paper
“Indeed, the selective and specific removal of mitochondria in senescent cells normalizes ROS levels [215].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [215]
In the citing paper
“Mitochondrial dysfunction is the main cause of elevated ROS production in senescence.”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [215]
In the citing paper
“Together, these observations support for the idea that muscle mitochondria are important regulators of muscle size.”
From Mitochondria initiate and regulate sarcopenia (2017) · cites this paper as [31]
In the citing paper
“a knockout of Mfn 1/2 in skeletal muscle, which prevented mitochondrial fusion, increased the accumulation of mtDNA defects and resulted in muscle atrophy (31).”
From Mitochondria initiate and regulate sarcopenia (2017) · cites this paper as [31]
In the citing paper
“Recently, Correia‐Melo et al. (2016) reported that DNA damage response (DDR) [induced by stress (i.e., ROS) or cell replication] activates mitochondrial biogenesis which will mediate a cell cycle arrest.”
From Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2-independent mechanism (2017) · cites this paper as Correia‐Melo et al. (2016)
In the citing paper
“Interestingly, they showed that the reduction in mitochondrial content by mTORC1 inhibition prevents cellular senescence.”
From Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2-independent mechanism (2017) · cites this paper as Correia‐Melo et al. (2016)
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Metadata
- Authors
- Correia‐Melo, C., Marques, F. D., Anderson, R., Hewitt, G., Hewitt, R., Cole, J., Carroll, B. M., Miwa, S., Birch, J., Merz, A., Rushton, M. D., Charles, M., Jurk, D., Tait, S. W., Czapiewski, R., Greaves, L., Nelson, G., Bohlooly‐Y, M., Rodriguez‐Cuenca, S., Vidal‐Puig, A., Mann, D., Saretzki, G., Quarato, G., Green, D. R., Adams, P. D., von Zglinicki, T., Korolchuk, V. I., & Passos, J. F.
- Affiliations
- Universidade do Porto (PT)
- Newcastle University (GB)
- Cancer Research UK Scotland Institute (GB)
- Wellcome Centre for Mitochondrial Research (GB)
- AstraZeneca (Sweden) (SE)
- University of Cambridge (GB)
- St. Jude Children's Research Hospital (US)
- Corresponding author
- Passos, João F
- ORCID
- Correia‐Melo, Clara
- Hewitt, Graeme
- Cole, John
- Carroll, Bernadette M
- Miwa, Satomi
- Birch, Jodie
- Charles, Michelle
- Jurk, Diana
- Tait, Stephen WG
- Czapiewski, Rafal
- Greaves, Laura
- Nelson, Glyn
- Bohlooly‐Y, Mohammad
- Vidal‐Puig, Antonio
- Mann, Derek
- Saretzki, Gabriele
- Quarato, Giovanni
- Green, Douglas R
- Adams, Peter D
- Korolchuk, Viktor I
- Passos, João F
- Venue
- The EMBO Journal
- Published
- 2016-02-04
- Volume
- 35
- Issue
- 7
- Pages
- 724-742
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC4818766
- OpenAlex
- W2267737556
- Cited by
- 796
- References
- 66
- Citations by year
- 2026: 71 · 2025: 104 · 2024: 91 · 2023: 83 · 2022: 82 · 2021: 92 · 2020: 74 · 2019: 59 · 2018: 66 · 2017: 48 · 2016: 25
- FWCI
- 53.15
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- The EMBO Journal (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Explore Bristol Research (publishedVersion, cc-by)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (acceptedVersion)
- Bristol Research (University of Bristol) (submittedVersion, cc-by)
- Newcastle University ePrints (Newcastle Univesity) (cc-by)
- Funders
- FP7‐MITIN (HEALTH‐F4‐2008‐223450)
- Medical Research Council Centre for Obesity and Related Metabolic Diseases
- BBSRC (BB/I020748/1, BB/K019260/1, BB/H022384/1, BB/K017314/1)
- Royal Society University Fellowship
- Foundation for Science and Technology (FCT), Portugal
- GABBA Program
- University of Porto
- Newcastle University
- David Phillips Fellowship
- AstraZeneca
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- cellular senescence, mitochondria, aging, pro-inflammatory phenotype, mitochondrial biogenesis, PGC-1β, mTORC1, ATM, Akt, DNA damage response, reactive oxygen species, glycolysis, cell cycle arrest, transcriptomics
- MeSH terms
- Aging, Animals, Cell Line, Humans, Mitochondria, Models, Biological, Phenotype, Mice
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