The DOI matches its Crossref record; 66 of the 66 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
The cited source says what the claim attributes to it.
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
The cited source says what the claim attributes to it.
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)
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
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
Flagged first, then by citations
Cited by
Sorted by citations
Items 701–794 of 794
Tian, X., Li, J., Zhang, Y., Gao, Y. J., Afzal, M. W., Wang, A., James, T. D., Bai, Y., & Guo, Y. (2021) · SSRN Electronic Journal · doi:10.2139/ssrn.3997563
Wang, T., Peng, W., Zhang, F., Wang, L., Zhang, J., Dong, W., Ye, C., Tian, X., Li, Y., & Gong, Y. (2020) · doi:10.21203/rs.3.rs-17046/v1
Topisirović, I. (2019) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.727678532.793561694
Immune Senescence and Inflammaging in Neurological Diseases
Baden, P., Cicco, S. D., Yu, C., & Deleidi, M. (2017) · Springer eBooks · doi:10.1007/978-3-319-64597-1_143-1
Ishaq, A., & Saretzki, G. C. (2022) · Recent Progress in Nutrition · doi:10.21926/rpn.2203016
Self-citationQuiescencia y senescencia: enfoque traslacional al paciente oncológico y críticamente enfermo.
Moscoso, S. X. A., Montalvo-Villagómez, M., González, F. E. J., Páez, P. A. V., Montero, C. G. V., & Vélez-Páez, J. L. (2019) · Revista Ecuatoriana de Ciencia Tecnología e Innovación en Salud Pública · doi:10.31790/inspilip.v4i1.154
An Overview of the Role of Senescence in Cancer
Al-Janabi, I. I. (2022) · Al-Rafidain Journal of Medical Sciences · doi:10.54133/ajms.v3i.77
NIH SenNet Consortium: Mapping Senescent Cells in the Human Body to Understand Health and DiseasePreprint
Lee, P. J., Blood, P. D., Börner, K., Campisi, J., Chen, F., Daldrup-Link, H. E., Jager, P. L. D., Ding, L., Duncan, F. E., Eickelberg, O., et al. (2022) · Preprints.org · doi:10.20944/preprints202207.0160.v2
Self-citationCellular senescence during aging
von Zglinicki, T. (2022) · Elsevier eBooks · doi:10.1016/b978-0-12-823761-8.00017-3
Telomeres and cell homeostasis in aging
Victorelli, S. G., & Passos, J. F. (2022) · Elsevier eBooks · doi:10.1016/b978-0-12-823761-8.00029-x
Self-citationKim, J. Y., Atanassov, I., Dethloff, F., Kroczek, L., & Langer, T. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.10.13.512077
Elimination of Senescent Cells by Polyphenols and Flavonoids
Harald, A. K. (2022) · Handbook of Oxidative Stress in Cancer: Therapeutic Aspects · doi:10.1007/978-981-16-5422-0_1
Hypotheses on the extended phenotype of the mitochondrion: sex, mortality, and agingPreprint
Irlam, G. (2023) · doi:10.32942/x2h309
The Third Annual Symposium of the Midwest Aging Consortium
Keller, A. R., Bai, H., Budinger, S., Eliazer, S., Hansen, M., Konopka, A. R., Morales‐Nebreda, L., Najt, C. P., Prahlad, V., Victorelli, S. G., et al. (2023) · The Journals of Gerontology Series A · doi:10.1093/gerona/glad239 · Cited by 1
Meas, S. J., Daire, G. M., Friedman, M. A., DeNapoli, R. C., Ghosh, P., Farr, J. N., & Donahue, H. J. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.10.09.561510
Insights into protein-bound uremic toxins in proximal tubule cell senescence and kidney fibrosis
Yang, Y. (2023) · Utrecht University Repository (Utrecht University) · doi:10.33540/1996
The Aging of Cells: Cellular Senescence and Implications for Age-Related Diseases
Kim, A., & Yoo, J. (2023) · Journal of Student Research · doi:10.47611/jsrhs.v12i3.4847
Marmisolle, I., Chacón, E., Mansilla, S., Bresque, M., Martínez, J., Martínez‐Zamudio, R. I., Herbig, U., Liu, J., Finkel, T., Escande, C., et al. (2024) · SSRN Electronic Journal · doi:10.2139/ssrn.4775691
Olovnikov, telomeres and telomerase. is it possible to prolong a healthy life?
Yegorov, Y. E. (2023) · Biochemistry (Moscow) · doi:10.31857/s0320972523110040
Darabi, F. L. A., Dehdar, M., & Azizi‐Tabesh, G. (2024) · International Journal of Cancer Management · doi:10.5812/ijcm-147476
WITHDRAWN: Mitochondria-linked lncRNAs: Unraveling their role in age-related disease
Shu, A., Jiang, Y., Tian, X., Yue, J., & Liu, Y. (2024) · Gene Reports · doi:10.1016/j.genrep.2024.102099
Retracted37 kDa LRP::FLAG enhances telomerase activity and reduces ageing markers in vivo
Otgaar, T. C., Bernert, M., Morris, G., Baichan, P., Bignoux, M. J., Letsolo, B. T., Weiss, S. F. T., & Ferreira, E. (2025) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-025-05593-0
Kong, B. S., L’Yi, S., Ramirez-Hernandez, E. G., Hong, S., Weidenspointner, R., Song, S., Caserta, C., Cho, Y. M., & Kory, N. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.04.09.647991
Noureen, N., & Kang, M. H. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.05.21.655338
Activation of pro-survival autophagy by a small molecule promoting p62 oligomerization
Panek, J., Fielder, E., Sun, C., Crabtree, S., Kataura, T., Wilson, N., Baheerathan, L., Tang, J., Booth, L. K., Yue, W. W., et al. (2026) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2026.113430
Self-citationYagi, I., Masui, R., Kato, E., Uchida, S., Sato, A., Ishigami, A., Gao, B., & Lim, C. T. (2025) · IEEE Sensors Journal · doi:10.1109/jsen.2025.3576789
Gao, L., Zhao, S., Liu, H., Sui, M., Xue, Y., Wang, B.-H., Zhang, T., Ding, H., Wang, X., Qi, J., et al. (2025) · Research Square · doi:10.21203/rs.3.rs-6947364/v1
C-C chemokine ligand 5 from women subcutaneous adipose tissue has a central role in vascular aging
Pelletier, L., Ayissi, K. N., Gorwood, J., Capel, É., Morichon, R., Mantecon, M., Auclair, M., Alili, R., Katlama, C., Cuzin, L., et al. (2025) · Cardiovascular Diabetology · doi:10.1186/s12933-025-02815-4
Wang, M., Liu, L., Liu, Y., Zhao, Y., & Yu, S. (2025) · Clinical and Experimental Medicine · doi:10.1007/s10238-025-01911-9
Proteomics-based mechanism of HIIT regulation of hepatic metabolism in aging female rats
He, J., Wang, Z., Qiao, Y., Zhang, C., Yu, Z., Ni, P., Zhao, Z., Jianmei, C., & Li, F. (2025) · Biogerontology · doi:10.1007/s10522-025-10351-7
Matus, J., Puebla-Huerta, A., Morgado-Cáceres, P., Quezada-Gutiérrez, C., Casanova-Canelo, C., Rosales‐Rojas, R., Lopez-Dominguez, J. A., Marín, I., Niño, S. A., Cruz, P., et al. (2025) · Research Square · doi:10.21203/rs.3.rs-8172868/v1
Alaidaroos, N. Y. A., Alraies, A., Waddington, R. J., Sloan, A. J., & Moseley, R. (2021) · Figshare · doi:10.6084/m9.figshare.14053068
Alaidaroos, N. Y. A., Alraies, A., Waddington, R. J., Sloan, A. J., & Moseley, R. (2021) · Figshare · doi:10.6084/m9.figshare.14053074
Alaidaroos, N. Y. A., Alraies, A., Waddington, R. J., Sloan, A. J., & Moseley, R. (2021) · Figshare · doi:10.6084/m9.figshare.14053062
Alaidaroos, N. Y. A., Alraies, A., Waddington, R. J., Sloan, A. J., & Moseley, R. (2021) · Figshare · doi:10.6084/m9.figshare.14053077
Alaidaroos, N. Y. A., Alraies, A., Waddington, R. J., Sloan, A. J., & Moseley, R. (2021) · Figshare · doi:10.6084/m9.figshare.14053071
Puebla-Huerta, A., Morgado-Cáceres, P., Gutierez, C. Q., Casanova-Canelo, C., Rosales-Rojas, R., López-Domínguez, J. A., Marin, I., Niño, S. A., Cruz, P., Saldivia-Piña, M., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2025.12.05.692660
Thoms, H. C., Brant, T. S., Duckett, K., Yang, Y., Dong, J., Wang, H., Derby, F., Akeke, O. F., Al‐Alayeen, F., Newell, A. S., et al. (2025) · Aging Cell · doi:10.1111/acel.70334
Self-citationMitokondriyal Disfonksiyonun Yaşlanmadaki Rolü
Kömüroğlü, A. U. (2025) · Özgür Yayınları eBooks · doi:10.58830/ozgur.pub1069.c4207
Dual targeting of PDPK1 and BRAF V600E is synthetically lethalPreprint
Khaket, T. P., Ghosh, C., Yang, Z., Boufraqech, M., Hu, J., Alamaw, E. D., Andrésson, Þ., O’Neill, M. J., Zhang, Y.-Q., Shen, M., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.03.15.711663
Liang, L., Liu, S., Li, Y., Zeng, F., He, Q., Wang, Z., Deng, J., & Zhou, Y. (2026) · Cell Communication and Signaling · doi:10.1186/s12964-026-02848-6 · Cited by 1
Zhang, X., Yang, L., He, X., Zhao, M., Fang, Z., Xu, G., Duan, Z., & Luo, K. (2026) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2026.03.050
Metabolic characterisation of skeletal muscle stem cells in distinct physiological states
Pala, F. (2017) · theses.fr (ABES) · doi:10.70675/ba751aadz6065z4221zbe6ez3b3e7cb993cc
de Freitas, J. A. N. L. F. (2020) · theses.fr (ABES) · doi:10.70675/0e6e3614z3915z4fb8za2cdz24b40b9679b2
Teissier, T. (2019) · theses.fr (ABES) · doi:10.70675/f49bc069z5ee6z4c49zb46fz0a1413dbba95
Caractérisation de la sénescence des cardiomyocytes et identification de marqueurs associés
Maggiorani, D. (2017) · theses.fr (ABES) · doi:10.70675/a58747bczd60bz4482za3b2z7ae33d26ffa4
Impact of aging on cardiac mesenchymal stromal cells
Martini, H. (2019) · theses.fr (ABES) · doi:10.70675/bb7ddcb3z0b6az4c39za6eczc94e0563f0a3
Mechanisms of precocious ageing in a human progeroid syndrome
Molina, C. F. (2021) · theses.fr (ABES) · doi:10.70675/f78c9fa2z621cz48b6zbf00z1133c36b723a
How Somatic Mutations cause Aging without Causing AgingPreprint
Wolf, A. M. (2026) · SSRN Electronic Journal · doi:10.2139/ssrn.6431458
Control of ependymal cell differentiation by the mTOR signaling pathway
Srivastava, A. (2021) · theses.fr (ABES) · doi:10.70675/0e4dc286zfb40z4d2bza4cdzd6fdff1cc2e8
Régulation de cohésine par le complexe TORC1 chez la levure Schizosaccharomyces pombe
Besson, D. (2024) · theses.fr (ABES) · doi:10.70675/9a8af873zd99dz4045z9287zb276eb60d7d4
Zhao, Z., Ou, Q., Zhu, J., He, Z., Yang, Y., Jiang, J., Wang, Q., Zhou, Y., Liu, Y., Zhu, X., et al. (2026) · Investigative Ophthalmology & Visual Science · doi:10.1167/iovs.67.4.30 · Cited by 1
Li, W., Liu, J., Fu, X., Liu, Y., Xu, Y., Fang, X., Guo, Q., & Liu, Q. (2026) · Archives of Pharmacal Research · doi:10.1007/s12272-026-01614-z
The p53/Mdm2 Pathway in Hepatocellular Carcinoma: From Molecular Pathogenesis to Targeted Therapies
Kirkness, K., & Mann, D. A. (2026) · Livers · doi:10.3390/livers6030039
Self-citationNADPH Oxidases and Pulmonary Fibrosis
Deskin, B., & Thannickal, V. J. (2026) · Springer eBooks · doi:10.1007/978-3-032-21135-4_22
Nuclear DNA Damage Response Triggers Reorganization of Mitochondrial Nucleic AcidsPreprint
Yu, C., Evens, E., Tchiong, S., Albinagorta, M. C., Okletey, J., & Tigano, M. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.05.23.727397
Diverse Forms of Autophagy and Their Roles in Liver Disease and Aging: A Comprehensive Review
Heo, S., Lee, M. Y., Jeong, C. Y., Kim, D. J., & Jun, J. H. (2026) · Proteomes · doi:10.3390/proteomes14020028
Phang, H. J., Arciniega, A., Bergstrom, J., Avalon, N. E., Glukhov, E., Gerwick, W. H., & Molina, A. J. A. (2026) · Oxidative Medicine and Cellular Longevity · doi:10.1155/omcl/9524037
Bingche, X., Hui, H., Lin, Y., Jiang, B., & Miao, H. (2026) · Current Opinion in Physiology · doi:10.1016/j.cophys.2026.100960
Zhang, H., Wang, Y., Wang, C., Guo, X., Chen, H., Hou, Y., Wu, X., Wu, Z.-J., Pan, W., Ma, R.-J., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.05.27.728315
Belhac, V., Dillingham, A., Coward, E., Teal, B., Turner, M. C., Gagnon, S. D., Qian, J., Wilford, H., Warren, E., Moger, N., et al. (2026) · Aging Cell · doi:10.1111/acel.70589 · Cited by 1
Self-citationMyelin Repair as a Neuroprotective Strategy for Multiple Sclerosis: From Bench to Bedside
Battah, T., Mastorodemos, V., Struecker, E., Mitsikostas, D. D., & Papadopoulos, D. (2026) · Medicina · doi:10.3390/medicina62061183
Yaşlanma Kader mi? Yaşlanma Biyolojisi ve Genetiği
Lüleyap, H. Ü. (2026) · Akademisyen Kitabevi eBooks · doi:10.37609/akya.4073
Orchestration of Autophagy and Senescence: Kinases Take the Center Stage
Basu, A. (2026) · Cells · doi:10.3390/cells15131176
Bidirectional modulation of aging-associated cellular phenotypes by mitochondrial genome replacementPreprint
Teruyama, F., Taya, T., Shikuma, A., Matoba, S., Numajiri, K., Umetani, S., Chen, Y., Peled, A., Galun, E., Assy, N., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.06.26.734763
Takayama, S., Cameron, S., Kuchta, K., Ishii, T., & Terada, M. (2026) · Frontiers in Physics · doi:10.3389/fphy.2026.1797094
Weston, M. S., Domínguez-Prieto, M., & Moisoi, N. (2026) · Cellular Signalling · doi:10.1016/j.cellsig.2026.112763
Melatonin Preserves Mitochondrial Redox Balance in UVB-Exposed Human Keratinocytes
Okura, M., Takaya, K., Ishii, T., Gagat, M., Wolnicka-Głubisz, A., Kishi, K., Okabe, K., Reiter, R. J., Slominski, A. T., & Kleszczyński, K. (2026) · Antioxidants · doi:10.3390/antiox15080939
Vázquez-Villaseñor, I., Benson, B. C., Richardson, C. D., Waller, R., Castelli, L. M., Simpson, J. E., Matthews, F. E., Brayne, C., & Wharton, S. B. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27156964
Mitochondrial regulation of cellular senescence heterogeneity
Ahn, M., Yoon, S.-J., & Seo, J. H. (2026) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2026.1866640
Etrouth, S., Zhu, Y., & Zhang, D. (2026) · Journal of Respiration · doi:10.3390/jor6030021
Khin, P. P., Mo, H. M. M., & Kim, C. (2026) · Antioxidants · doi:10.3390/antiox15091061
Papp, G., Arany, A. C., Diós, Á., Gyetvai, Á., Nagy, A., Csiki, Z., & Balogh, L. (2026) · Medical Sciences · doi:10.3390/medsci14050538
Genotoxic and metabolic stress drive divergent senescence programs in human microgliaPreprint
Jose, N. V., Janssens, S., Kang, E., & Platt, B. (2026) · Research Square · doi:10.21203/rs.3.rs-10751142/v1
Vaping reorganizes the pulmonary macrophage landscape into multiple sex-dimorphic microenvironments
Phillips, J. A., Schwartz, A. V., Nguyen, A. D., Echeagaray, O., Sussman, M. A., & George, U. Z. (2026) · Molecular Immunology · doi:10.1016/j.molimm.2026.08.013
Breaking the self-reinforcing cycle of aging: Biomaterial strategies for aged bone regeneration
Wang, Y., Chen, J., Liu, X., Pei, Y., Chen, S., & Zhou, Y. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103348
Metabolism licenses the senescence secretome
Picallos-Rabina, P., & Demaria, M. (2026) · Cell Research · doi:10.1038/s41422-026-01295-9
Multidimensional Regulatory Network of Cellular Senescence: From Mechanisms to Theranostics
Lv, Z., Liu, Y., Liu, Y., Tan, Y., Man, Y., Shuqing, D., Zhang, Z., Lee, L. P., Chen, Q., & Liu, Z. (2026) · ACS Biomaterials Science & Engineering · doi:10.1021/acsbiomaterials.6c00849
Quantitative proteomics reveals coordinated changes in the proteome during replicative senescence
Fernandes, N. D. S., Kielisch, F., Fulzele, A., Karunanithi, S., Gräf, J. F., Chen, J., Behl, C., Ulrich, H. D., & Beli, P. (2026) · Nature Communications · doi:10.1038/s41467-026-77686-8
The role of senescence in kidney ageing, injury and fibrosis
Janas, P. P., Mason, T., & Ferenbach, D. A. (2026) · Nature Reviews Nephrology · doi:10.1038/s41581-026-01123-8
Zhi, D., Wu, D., Xu, H., Liang, H., Zhu, D., 彭舒畅, Tong, B., Lei, J., Zhou, X., Wang, H., et al. (2026) · Cell Death and Differentiation · doi:10.1038/s41418-026-01864-w
Elamipretide Rejuvenates Oocyte Quality and Restores Female Fertility During Reproductive Aging
Zhang, H., Wang, Y., Wang, C., Guo, X., Chen, H., Hou, Y., Wu, X., Wu, Z., Pan, W., Ma, R., et al. (2026) · Aging Cell · doi:10.1111/acel.70749
Furlan, G., da Silva, J. B., Hoshino, L. V. D. C., Baesso, M. L., Simas, F. F., & Bruschi, M. L. (2026) · ACS Omega · doi:10.1021/acsomega.6c06908
Mohamad, S., McGuinness, M. K., Zhou, Y., Jiang, X., Casirati, G., Mucci, A., Nunes, S. C., Shimamura, A., Genovese, P., & Williams, D. A. (2026) · JCI Insight · doi:10.1172/jci.insight.209595
Luo, Y., Yu, H., Zhang, J., Wu, Z., & Zhang, H. (2026) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2026.1991837
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
