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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
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
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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Kim, D., Pertea, G., Trapnell, C., Pimentel, H., Kelley, R., & Salzberg, S. L. (2013) · Genome Biology · doi:10.1186/gb-2013-14-4-r36 · Cited by 12,668
mTOR Signaling in Growth Control and Disease
Laplante, M., & Sabatini, D. M. (2012) · Cell · doi:10.1016/j.cell.2012.03.017 · Cited by 8,509
A biomarker that identifies senescent human cells in culture and in aging skin in vivo.
Dimri, G. P., Lee, X., Basile, G., Acosta, M., Scott, G., Roskelley, C., Medrano, E. E., Linskens, M., Rubelj, I., & Pereira-Smith, O. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.20.9363 · Cited by 7,477
Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
Narendra, D., Tanaka, A., Suen, D.-F., & Youle, R. J. (2008) · The Journal of Cell Biology · doi:10.1083/jcb.200809125 · Cited by 4,026
Rapamycin fed late in life extends lifespan in genetically heterogeneous mice
Harrison, D. E., Strong, R., Sharp, Z. D., Nelson, J. F., Astle, C. M., Flurkey, K., Nadon, N. L., Wilkinson, J. E., Frenkel, K., Carter, C. S., et al. (2009) · Nature · doi:10.1038/nature08221 · Cited by 3,766
Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders
Baker, D. J., Wijshake, T., Tchkonia, T., LeBrasseur, N. K., Childs, B. G., van de Sluis, B., Kirkland, J. L., & van Deursen, J. M. (2011) · Nature · doi:10.1038/nature10600 · Cited by 3,670 · cited 1×
“Cellular senescence, the irreversible loss of proliferative potential in somatic cells, has been shown to not only play a major role in tumour suppression, but also to contribute to age-related tissue degeneration (Baker et al , 2011).”
Differential analysis of gene regulation at transcript resolution with RNA-seq
Trapnell, C., Hendrickson, D. G., Sauvageau, M., Goff, L., Rinn, J. L., & Pachter, L. (2013) · Nature Biotechnology · doi:10.1038/nbt.2450 · Cited by 3,492
TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling
Inoki, K., Li, Y., Zhu, T., Wu, J., & Guan, K.-L. (2002) · Nature Cell Biology · doi:10.1038/ncb839 · Cited by 3,083
A DNA damage checkpoint response in telomere-initiated senescence
Fagagna, F. D. D., Reaper, P. M., Clay-Farrace, L., Fiegler, H., Carr, P., von Zglinicki, T., Saretzki, G., Carter, N. P., & Jackson, S. P. (2003) · Nature · doi:10.1038/nature02118 · Cited by 2,917 · cited 1×
“Activation of a DDR is a prominent initiator of senescence during stress-induced (Passos et al , 2010), replicative (d’Adda di Fagagna et al , 2003) and oncogene-induced senescence (OIS) (Suram et al , 2012).”
Self-citationPINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1
Geisler, S., Holmström, K. M., Skujat, D., Fiesel, F. C., Rothfuss, O. C., Kahle, P. J., & Springer, W. (2010) · Nature Cell Biology · doi:10.1038/ncb2012 · Cited by 2,835
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Battram, A. M., Bachiller, M., & Martín-Antonio, B. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21124346 · Cited by 66
Human aging DNA methylation signatures are conserved but accelerated in cultured fibroblasts
Sturm, G., Cardenas, A., Bind, M.-A., Horvath, S., Wang, S., Wang, Y., Hägg, S., Hirano, M., & Picard, M. (2019) · Epigenetics · doi:10.1080/15592294.2019.1626651 · Cited by 61
Li, Y., Berliocchi, L., Li, Z., & Rasmussen, L. J. (2023) · Aging Cell · doi:10.1111/acel.13942 · Cited by 66
Tanaka, H., Takebayashi, S., Sakamoto, A., Igata, T., Nakatsu, Y., Saitoh, N., Hino, S., & Nakao, M. (2017) · Cell Reports · doi:10.1016/j.celrep.2017.02.021 · Cited by 58
The Emerging Role of Senescence in Ocular Disease
Sreekumar, P. G., Hinton, D. R., & Kannan, R. (2020) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2020/2583601 · Cited by 67
Effects of GH/IGF on the Aging Mitochondria
Poudel, S. B., Dixit, M., Neginskaya, M. A., Nagaraj, K., Pavlov, E. V., Werner, H., & Yakar, S. (2020) · Cells · doi:10.3390/cells9061384 · Cited by 61
Self DNA perpetuates IPF lung fibroblast senescence in a cGAS-dependent manner
Schuliga, M. J., Read, J. M., Blokland, K. E. C., Waters, D. W., Burgess, J. K., Prêle, C. M., Mutsaers, S. E., Jaffar, J., Westall, G. P., Reid, A. T., et al. (2020) · Clinical Science · doi:10.1042/cs20191160 · Cited by 61
Ageing mechanisms that contribute to tissue remodeling in lung disease
Schuliga, M. J., Read, J. M., & Knight, D. A. (2021) · Ageing Research Reviews · doi:10.1016/j.arr.2021.101405 · Cited by 62
Depletion of mitochondria in mammalian cells through enforced mitophagy
Correia‐Melo, C., Ichim, G., Tait, S. W. G., & Passos, J. F. (2016) · Nature Protocols · doi:10.1038/nprot.2016.159 · Cited by 63
Self-citationRoadmap for alleviating the manifestations of ageing in the cardiovascular system
Liberale, L., Tual-Chalot, S., Sedej, S., Ministrini, S., Georgiopoulos, G., Grunewald, M., Bäck, M., Bochaton-Piallat, M.-L., Boon, R. A., Ramos, G. C., et al. (2025) · Nature Reviews Cardiology · doi:10.1038/s41569-025-01130-5 · Cited by 59
Self-citationCellular Senescence in Liver Disease and Regeneration
Ferreira-González, S., Rodrigo‐Torres, D., Gadd, V. L., & Forbes, S. J. (2021) · Seminars in Liver Disease · doi:10.1055/s-0040-1722262 · Cited by 60
Mitophagy in aging and longevity
Guo, J., & Chiang, W. (2021) · IUBMB Life · doi:10.1002/iub.2585 · Cited by 60
Wang, Y., Wang, H., Zhuo, Y., Hu, Y., Zhang, Z., Ye, J., Liu, L., Luo, L., Zhao, C., Zhou, Q., et al. (2020) · Aging · doi:10.18632/aging.103587 · Cited by 58
Hu, H., Zhao, R., He, Q., Cui, C., Song, J., Guo, X., Zang, N., Yang, M., Zou, Y., Yang, J., et al. (2022) · The FASEB Journal · doi:10.1096/fj.202101988r · Cited by 61
Gu, Y., Zhao, X., Zhang, N., Yang, Y., Yi, Y., Shao, Q.-H., Liu, M.-X., & Zhang, X.-L. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102577 · Cited by 60
Functional Significance of the Mitochondrial Membrane Potential
Zorova, L. D., Popkov, V. A., Plotnikov, E. Y., Silachev, D. N., Pevzner, I. B., Jankauskas, S. S., Zorov, S. D., Babenko, V. А., & Zorov, D. B. (2018) · Biochemistry (Moscow) Supplement Series A Membrane and Cell Biology · doi:10.1134/s1990747818010129 · Cited by 59
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Madreiter‐Sokolowski, C. T., Sokolowski, A., Waldeck‐Weiermair, M., Malli, R., & Graier, W. F. (2018) · Genes · doi:10.3390/genes9030165 · Cited by 61
The Roles of Mitochondrial Dysfunction and Reactive Oxygen Species in Aging and Senescence
Zia, A., Farkhondeh, T., Pourbagher‐Shahri, A. M., & Samarghandian, S. (2021) · Current Molecular Medicine · doi:10.2174/1566524021666210218112616 · Cited by 70
Telomeres, cellular senescence, and aging: past and future
Eppard, M., Passos, J. F., & Victorelli, S. G. (2023) · Biogerontology · doi:10.1007/s10522-023-10085-4 · Cited by 67
Self-citationNacarelli, T., Azar, A., Altinok, O., Orynbayeva, Z., & Sell, C. (2018) · GeroScience · doi:10.1007/s11357-018-0030-2 · Cited by 57
Giuliani, A., Cirilli, I., Prattichizzo, F., Mensa’, E., Fulgenzi, G., Sabbatinelli, J., Graciotti, L., Olivieri, F., Procopio, A. D., Tiano, L., et al. (2018) · Aging · doi:10.18632/aging.101591 · Cited by 58
Saito, N., Araya, J., Ito, S., Tsubouchi, K., Minagawa, S., Hara, H., Ito, A., Nakano, T., Hosaka, Y., Ichikawa, A., et al. (2019) · The Journal of Immunology · doi:10.4049/jimmunol.1801293 · Cited by 58
Translational Control during Cellular Senescence
Payea, M. J., Anerillas, C., Tharakan, R., & Gorospe, M. (2020) · Molecular and Cellular Biology · doi:10.1128/mcb.00512-20 · Cited by 56
Lionaki, E., Gkikas, I., Daskalaki, I., Ioannidi, M.-K., Klapa, M. I., & Tavernarakis, N. (2022) · Nature Communications · doi:10.1038/s41467-022-28272-1 · Cited by 56
The mitochondria in lung fibrosis: friend or foe?
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Huang, J., Meng, P., Wang, C., Zhang, Y., & Zhou, L. (2022) · Theranostics · doi:10.7150/thno.70588 · Cited by 54
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Wang, S., Wang, Q., Wang, H., Qin, C., Cui, X., Li, L., Liu, Y., & Chang, H. (2019) · Pharmaceutical Biology · doi:10.1080/13880209.2019.1628073 · Cited by 53
Chang, A. C. Y., Pardon, G., Chang, A. C. H., Wu, H., Ong, S., Eguchi, A., Ancel, S., Holbrook, C., Ramunas, J., Ribeiro, A. J. S., et al. (2021) · Stem Cell Reports · doi:10.1016/j.stemcr.2021.04.018 · Cited by 54
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Gao, Y. Q., Cai, W., Zhou, Y., Li, Y., Cheng, J., & Wei, F. (2022) · Inflammation Research · doi:10.1007/s00011-022-01649-0 · Cited by 53
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Salmonowicz, H., & Passos, J. F. (2017) · Aging Cell · doi:10.1111/acel.12580 · Cited by 54
Self-citationSeo, S.-W., Park, S.-K., Oh, S. J., & Shin, O. S. (2018) · PLoS ONE · doi:10.1371/journal.pone.0202323 · Cited by 54
Hou, J., Yun, Y. J., Xue, J., Jeon, B.-M., & Kim, S. (2020) · Phytotherapy Research · doi:10.1002/ptr.6636 · Cited by 53
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Wang, X., Zhang, J., Xiu, C., Yang, J., Fang, J., & Lei, Y. (2020) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2020/7151946 · Cited by 51
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Self-citationWalters, H., & Cox, L. S. (2021) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2021/6697861 · Cited by 51
Malvaso, A., Gatti, A., Negro, G., Calatozzolo, C., Medici, V., & Poloni, T. E. (2023) · Cells · doi:10.3390/cells12242824 · Cited by 54
Biphasic Modeling of Mitochondrial Metabolism Dysregulation during Aging
Baker, D. J., & Peleg, S. (2017) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2017.06.005 · Cited by 48
Melatonin prevents lung injury by regulating apelin 13 to improve mitochondrial dysfunction
Zhang, L., Li, F., Su, X., Li, Y., Wang, Y., Fang, R., Guo, Y., Jin, T., Shan, H., Zhao, X., et al. (2019) · Experimental & Molecular Medicine · doi:10.1038/s12276-019-0273-8 · Cited by 49
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Venosa, A. (2020) · Frontiers in Medicine · doi:10.3389/fmed.2020.606462 · Cited by 51
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Grootaert, M. O. J. (2024) · npj Aging · doi:10.1038/s41514-024-00170-4 · Cited by 56
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von Zglinicki, T. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102558 · Cited by 57
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Tan, S., & Wong, E. S. P. (2017) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2017/9028435 · Cited by 47
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Scialò, F., & Sanz, A. (2021) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2021.01.018 · Cited by 48
Hao, X., Bu, W., Lv, G., Xu, L., Hou, D., Wang, J., Liu, X., Yang, T., Zhang, X., Liu, Q., et al. (2021) · Oncogene · doi:10.1038/s41388-021-02105-9 · Cited by 46
Song, M. J., Park, C., Kim, H., Han, S., Lee, S., Lee, D. H., & Chung, J. H. (2023) · Aging Cell · doi:10.1111/acel.14000 · Cited by 47
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Li, Y., Zhang, H., Yu, C., Dong, X., Yang, F., Wang, M., Wen, Z., Su, M., Li, B., & Yang, L. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25189975 · Cited by 48
Galea, G. L., Meakin, L. B., Harris, M. A., Delisser, P., Lanyon, L. E., Harris, S. E., & Price, J. S. (2016) · Gene · doi:10.1016/j.gene.2016.11.006 · Cited by 46
Mechanisms driving the ageing heart
Anderson, R., Richardson, G. D., & Passos, J. F. (2017) · Experimental Gerontology · doi:10.1016/j.exger.2017.10.015 · Cited by 47
Self-citationKim, S. R., Eirin, A., Zhang, X., Lerman, A., & Lerman, L. O. (2019) · Cellular Physiology and Biochemistry · doi:10.33594/000000044 · Cited by 44
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You, Y., Yuan, H., Min, H., Li, C. R., & Chen, J. (2023) · Journal of Hazardous Materials · doi:10.1016/j.jhazmat.2023.132489 · Cited by 44
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Vecoli, C., Borghini, A., & Andreassi, M. G. (2020) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2020.108309 · Cited by 47
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Choudhury, D., Rong, N., Ikhapoh, I. A., Rajabian, N., Tseropoulos, G., Wu, Y., Mehrotra, P., Thiyagarajan, R., Shahini, A., Seldeen, K. L., et al. (2022) · Cell Reports · doi:10.1016/j.celrep.2022.111744 · Cited by 44
Pini, M., Czibik, G., Sawaki, D., Mezdari, Z., Braud, L., Delmont, T., Mercedes, R., Martel, C., Buron, N., Marcelin, G., et al. (2021) · Aging Cell · doi:10.1111/acel.13421 · Cited by 43
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Qin, Y., Liu, H., & Wu, H. (2025) · Pharmaceuticals · doi:10.3390/ph18020244 · Cited by 47
Qiu, X., Guo, H., Yang, J., Ji, Y., Wu, C., & Chen, X. (2018) · Scientific Reports · doi:10.1038/s41598-018-19828-7 · Cited by 41
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Chaudhari, S. N., & Kipreos, E. T. (2018) · BioEssays · doi:10.1002/bies.201800005 · Cited by 42
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Hartman, R. A., Patil, P., Tisherman, R. T., Croix, C. M. S., Niedernhofer, L. J., Robbins, P. D., Ambrosio, F., Houten, B. V., Sowa, G., & Vo, N. N. (2018) · European Cells and Materials · doi:10.22203/ecm.v036a13 · Cited by 42
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Sikora, E., Bielak-Żmijewska, A., & Mosieniak, G. (2018) · Postępy Biochemii · doi:10.18388/pb.2018_120 · Cited by 45
Bourdens, M., Jeanson, Y., Taurand, M., Juin, N., Carrière, A., Clément, F., Casteilla, L., Bulteau, A., & Planat‐Benard, V. (2019) · Scientific Reports · doi:10.1038/s41598-019-45191-2 · Cited by 46
Crochemore, C., Molina, C. F., Montagne, B., Salles, A., & Ricchetti, M. (2019) · Nature Communications · doi:10.1038/s41467-019-13314-y · Cited by 41
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Rocchi, A., Carminati, E., Fusco, A. D., Kowalska, J. A., Floß, T., & Benfenati, F. (2021) · Aging Cell · doi:10.1111/acel.13471 · Cited by 42
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Strzeszewska, A., Alster, O., Mosieniak, G., Ciolko, A., & Sikora, E. (2018) · Cell Death and Disease · doi:10.1038/s41419-017-0069-5 · Cited by 42
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Udomsinprasert, W., Sobhonslidsuk, A., Jittikoon, J., Honsawek, S., & Chaikledkaew, U. (2021) · Expert Opinion on Therapeutic Targets · doi:10.1080/14728222.2021.1992385 · Cited by 41
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Zheng, S., Zhu, L., Wu, L., Liu, H., Ma, X., Li, Q., Wu, M., Wang, W., Li, J., & Wu, H. (2022) · Helicobacter · doi:10.1111/hel.12944 · Cited by 42
Li, N., Ye, Y., Wu, Y., Li, L., Hu, J., Luo, D., Li, Y., Yang, J., Gao, Y., Hai, W., et al. (2023) · iScience · doi:10.1016/j.isci.2023.106571 · Cited by 44
Zhang, M., Cui, S., Mao, B., Zhang, Q., Zhao, J., Tang, X., & Chen, W. (2023) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.3c01062 · Cited by 45
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James, E. L., Lane, J. A. E., Michalek, R. D., Karoly, E. D., & Parkinson, E. K. (2016) · Scientific Reports · doi:10.1038/srep38489 · Cited by 43
Li, Q., Lu, H., Hu, G., Ye, Z., Zhai, D., Zhao, Y., Wang, L., An, X., & Lu, Z. (2019) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2019.03.194 · Cited by 43
Miller, K. N., Li, B., Pierce-Hoffman, H. R., Patel, S., Lei, X., Rajesh, A., Teneche, M. G., Havas, A. P., Gandhi, A., Macip, C. C., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-57229-3 · Cited by 47
Self-citationXu, L., Wu, T., Lu, S., Hao, X., Qin, J., Wang, J., Zhang, X., Liu, Q., Kong, B., Gong, Y., et al. (2020) · Redox Biology · doi:10.1016/j.redox.2020.101604 · Cited by 39
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Hassan, J. W., & Bhatwadekar, A. D. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.896907 · Cited by 39
Sienkiewicz, M., Sroka, K., Binienda, A., Jurk, D., & Fichna, J. (2023) · Ageing Research Reviews · doi:10.1016/j.arr.2023.102083 · Cited by 39
Self-citationParisi, M. M., Grün, L. K., Lavandoski, P., Alves, L. B., Bristot, I. J., Mattiello, R., Mottin, C. C., Klamt, F., Jones, M. H., Padoin, A. V., et al. (2017) · Obesity · doi:10.1002/oby.21888 · Cited by 40
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Kucheryavenko, O., Nelson, G., von Zglinicki, T., Korolchuk, V. I., & Carroll, B. (2019) · Biogerontology · doi:10.1007/s10522-019-09802-9 · Cited by 39
Self-citationMitochondrial Bioenergetics and Dynamics in Secretion Processes
Martínez, J., Marmisolle, I., Tarallo, D., & Quijano, C. (2020) · Frontiers in Endocrinology · doi:10.3389/fendo.2020.00319 · Cited by 41
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Mas‐Bargues, C., Borrás, C., & Viña, J. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22041527 · Cited by 39
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Mustafa, S., Pawar, J. S., & Ghosh, I. (2021) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2021.03.110 · Cited by 41
Estimation of the Mitochondrial Membrane Potential Using Fluorescence Lifetime Imaging Microscopy
Okkelman, I. A., Papkovsky, D. B., & Dmitriev, R. I. (2019) · Cytometry Part A · doi:10.1002/cyto.a.23886 · Cited by 38
Cavinato, M. S., Madreiter‐Sokolowski, C. T., Büttner, S., Schosserer, M., Zwerschke, W., Wedel, S., Grillari, J., Graier, W. F., & Jansen‐Dürr, P. (2020) · FEBS Journal · doi:10.1111/febs.15631 · Cited by 38
Cellular Senescence as the Key Intermediate in Tau-Mediated Neurodegeneration
Mendelsohn, A. R., & Larrick, J. W. (2018) · Rejuvenation Research · doi:10.1089/rej.2018.2155 · Cited by 39
Role of Oxidative Stress in the Senescence Pattern of Auditory Cells in Age-Related Hearing Loss
Chacón, L. D. M. R., Martínez-Rodríguez, S., Madrid, R., Yanes‐Diaz, J., Riestra‐Ayora, J., Fernández, R. S., & Sánchez‐Rodríguez, C. (2021) · Antioxidants · doi:10.3390/antiox10091497 · Cited by 37
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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