The DOI matches its Crossref record; 39 of the 39 references it cites were found in a registry or an index.
Autophagy mediates the mitotic senescence transition
Open accessAbstract
As a stress response, senescence is a dynamic process involving multiple effector mechanisms whose combination determines the phenotypic quality. Here we identify autophagy as a new effector mechanism of senescence. Autophagy is activated during senescence and its activation is correlated with negative feedback in the PI3K–mammalian target of rapamycin (mTOR) pathway. A subset of autophagy-related genes are up-regulated during senescence: Overexpression of one of those genes, ULK3, induces autophagy and senescence. Furthermore, inhibition of autophagy delays the senescence phenotype, including senescence-associated secretion. Our data suggest that autophagy, and its consequent protein turnover, mediate the acquisition of the senescence phenotype.
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“Some studies have touched on the functional relevance of autophagy in senescence, where its role appears to vary depending on cell type and senescence triggers (Patschan et al. 2007; Young et al. 2009; Leidal et al. 2012; Mosieniak et al. 2012; Singh et al. 2012; Dörr et al. 2013).”
From Cellular senescence and its effector programs (2014) · cites this paper as Young et al. 2009
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
“In preclinical models, proteotoxic stress not only drives entry into a senescent state, but also activates autophagy, which consequently buffers toxicity from misfolded SASP factors 44,45 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [44]
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
“they may have both similar and distinct functions that are tissue-or cell-type specific [637-641]”
From Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1 (2021) · cites this paper as [638]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The kinetics of these gene expression changes were similar to that of SASP components, implying some level of correlation between autophagy and the SASP.”
From Cellular senescence and its effector programs (2014) · cites this paper as Young et al. 2009
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In the citing paper
“We recently showed that autophagy is activated during the dynamic phase of OIS in HDFs, which was accompanied by a concerted up-regulation of genes involved in both autophagy and lysosomal biogenesis (Young et al. 2009).”
From Cellular senescence and its effector programs (2014) · cites this paper as Young et al. 2009
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In the citing paper
“Indeed, inhibition of autophagy suppressed the production of both IL6 and IL8 and delayed the establishment of senescence.”
From Cellular senescence and its effector programs (2014) · cites this paper as Young et al. 2009
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“ULK2 has a higher degree of identity with ULK1 than any of the other homologs”
From Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1 (2021) · cites this paper as [638]
Experimental — accuracy not yet measuredIn the citing paper
“macro-autophagy (hereafter referred to as autophagy)—a tightly regulated major lysosomal degradation pathway (27–30)—has been implicated in establishing the SASP through the target of rapamycin (TOR) autophagy spatial coupling compartment (TASCC).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [31]
In the citing paper
“Our results indicate that autophagy is both a negative and a positive regulator of senescence, resolving apparently contradictory reports in the literature (31–33, 44).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [31]
In the citing paper
“These cells use autophagy for their maintenance”
From p21 maintains senescent cell viability under persistent DNA damage response by restraining JNK and caspase signaling (2017) · cites this paper as Young et al, 2009
In the citing paper
“Autophagy is activated during senescence”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [59]
In the citing paper
“Autophagy is dynamically activated during OIS and facilitates the synthesis of interleukin 6 (IL-6) and IL-8, major components of the SASP 58,59 .”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [59]
In the citing paper
“and that the inhibition of autophagy delays of onset of senescence and SASP.”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [59]
In the citing paper
“Autophagy is also required for the execution of the senescence program because its inhibition delays the senescence-related cell cycle arrest and SASP factor accumulation, at least in OIS [244].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [244]
In the citing paper
“In senescence induced by oncogenic Ras, protein synthesis and autophagic degradation are simultaneous activated, and the same cell displays high autophagic activity and activated mTOR, the autophagy inhibitor [244].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [244]
In the citing paper
“Moreover, autophagy is required for some instances of cell-autonomous tumor suppression by senescence (e.g., in oncogene-induced senescence caused by HRAS V12 and BRAF V600E ) 156,157 and cell death (e.g., in the context of ferroptosis) 158 (Figure 3A).”
From Meta-hallmarks of aging and cancer (2023) · cites this paper as [156]
In the citing paper
“Of note, proficient autophagy is required for the successful establishment of OIS.156”
From Meta-hallmarks of aging and cancer (2023) · cites this paper as [156]
In the citing paper
“Although BNIP3L is typically thought of as pro-apoptotic [181], anti-apoptotic roles have been recently discovered, particularly in reactive astrocytes during ALS disease progression [35]. Similarly, BNIP3L has been shown to increase in senescent cells to direct mitochondria to autophagosomes for degradation [174].”
From Early onset senescence and cognitive impairment in a murine model of repeated mTBI (2021) · cites this paper as [174]
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Citations
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Metadata
- Authors
- Young, A. R. J., Narita, M., Ferreira, M., Kirschner, K., Sadaie, M., Darot, J. F. J., Tavaré, S., Arakawa, S., Shimizu, S., Watt, F. M., & Narita, M.
- Affiliations
- Cancer Research UK (GB)
- European Bioinformatics Institute (GB)
- Tokyo Medical and Dental University (JP)
- ORCID
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2009-03-11
- Volume
- 23
- Issue
- 7
- Pages
- 798-803
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC2666340
- OpenAlex
- W2113995129
- Cited by
- 1,078
- References
- 39
- Citations by year
- 2026: 19 · 2025: 36 · 2024: 53 · 2023: 56 · 2022: 62 · 2021: 90 · 2020: 64 · 2019: 52 · 2018: 70 · 2017: 64 · 2016: 78 · 2015: 60 · 2014: 78 · 2013: 86 · 2012: 72
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- Cancer Research UK (19556)
- University of Cambridge
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- 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
- Keywords
- autophagy, cellular senescence, PI3K/mTOR pathway, ULK3, protein turnover, negative feedback regulation, autophagy-related genes
- MeSH terms
- Aging, Autophagy, Gene Expression Regulation, Humans, Immunohistochemistry, Microtubule-Associated Proteins, Mitosis, Neoplasms, Protein Kinases, Protein Serine-Threonine Kinases, Feedback, Physiological, TOR Serine-Threonine Kinases
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 ›
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