The DOI matches its Crossref record.
How autophagy both activates and inhibits cellular senescence
Open accessAbstract
Autophagy and cellular senescence are stress responses essential for homeostasis. While recent studies indicate a genetic relationship between autophagy and senescence, whether autophagy acts positively or negatively on senescence is still subject to debate. Although autophagy was originally recognized as a nonspecific lysosomal degradation pathway (general autophagy), increasing evidence supports a selective form of autophagy that mediates the degradation of specific targets (selective autophagy). Our recent study revealed distinctive roles of selective autophagy and general autophagy in the regulation of senescence, at least in part resolving apparently contradictory reports regarding the relationship between these 2 important homeostatic stress responses.
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?
In the citing paper
“Senescent cells are generally characterized by increased lysosomal content occurring as a consequence of defective lysosomal turnover24 or of multi-faceted changes in autophagy25.”
From Algorithmic assessment of cellular senescence in experimental and clinical specimens (2021) · cites this paper as [25]
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
Cited by
Sorted by citations
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1
Klionsky, D. J., Abdel-Aziz, A. K., Abdelfatah, S., Abdellatif, M., Abdoli, A., Abel, S., Abeliovich, H., Abildgaard, M. H., Abudu, Y. P., Acevedo-Arozena, A., et al. (2021) · Autophagy · doi:10.1080/15548627.2020.1797280 · Cited by 2,897
Self-citationThe metabolic roots of senescence: mechanisms and opportunities for intervention
Wiley, C. D., & Campisi, J. (2021) · Nature Metabolism · doi:10.1038/s42255-021-00483-8 · Cited by 691
Jun, J.-I., & Lau, L. F. (2018) · Journal of Clinical Investigation · doi:10.1172/jci93563 · Cited by 358
Therapy-Induced Senescence: An “Old” Friend Becomes the Enemy
Saleh, T., Bloukh, S., Carpenter, V. J., Alwohoush, E., Bakeer, J., Darwish, S., Azab, B., & Gewirtz, D. A. (2020) · Cancers · doi:10.3390/cancers12040822 · Cited by 295
Molecular mechanisms of aging and anti-aging strategies
Li, Y., Tian, X., Luo, J., Bao, T., Wang, S., & Wu, X. (2024) · Cell Communication and Signaling · doi:10.1186/s12964-024-01663-1 · Cited by 380
“Increasing evidence indicates that intracellular lysosomal proteolytic function is impaired with aging in various model organisms, which impairs autophagic flux, exacerbates cell damage, and promotes the occurrence of aging-related diseases [155].”
Background
Metadata
- Authors
- Kang, C., & Elledge, S. J.
- Affiliations
- Brigham and Women's Hospital (US)
- Corresponding author
- Elledge, Stephen J.
- Venue
- Autophagy
- Publisher
- Informa UK Limited
- Published
- 2016-04-29
- Volume
- 12
- Issue
- 5
- Pages
- 898-899
- ISSN
- 1554-8627 (ISSN-L)
- 1554-8635
- PMC
- PMC4854549
- OpenAlex
- W2344541663
- Cited by
- 228
- References
- 0
- Citations by year
- 2026: 10 · 2025: 25 · 2024: 37 · 2023: 22 · 2022: 33 · 2021: 33 · 2020: 25 · 2019: 21 · 2018: 13 · 2017: 9
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Autophagy (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health
- 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
- cellular senescence, selective autophagy, lysosomal degradation, senescence regulation
- MeSH terms
- Animals, Autophagy, DNA Damage, Humans, Lysosomes, Phenotype, Cellular Senescence, GATA4 Transcription Factor
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