The DOI matches its Crossref record; 70 of the 70 references it cites were found in a registry or an index.
Cellular senescence and apoptosis: how cellular responses might influence aging phenotypes
Open accessAbstract
Aging in complex multi-cellular organisms such as mammals entails distinctive changes in cells and molecules that ultimately compromise the fitness of adult organisms. These cellular and molecular changes lead to the phenotypes we recognize as aging. This review discusses some of the cellular and molecular changes that occur with age, specifically changes that occur as a result of cellular responses that evolved to ameliorate the inevitable damage that is caused by endogenous and environmental insults. Because the force of natural selection declines with age, it is likely that these processes were never optimized during their evolution to benefit old organisms. That is, some age-related changes may be the result of gene activities that were selected for their beneficial effects in young organisms, but the same gene activities may have unselected, deleterious effects in old organisms, a phenomenon termed antagonistic pleiotropy. Two cellular processes, apoptosis and cellular senescence, may be examples of antagonistic pleiotropy. Both processes are essential for the viability and fitness of young organisms, but may contribute to aging phenotypes, including certain age-related diseases.
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 check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“magnetic resonance imaging (MRI) studies have shown that normal aging is associated with gray matter volume reductions and functional alterations in several regions critical for higher cognitive function: prefrontal, medial temporal and parietal cortices.21–24”
From Maintenance, reserve and compensation: the cognitive neuroscience of healthy ageing (2018) · cites this paper as [24]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“It is worth noting that young adults may also upregulate activity in response to increased task demands, but that the demand threshold for upregulation may be higher in young, compared to older adults24,36.”
From Maintenance, reserve and compensation: the cognitive neuroscience of healthy ageing (2018) · cites this paper as [24]
Experimental — accuracy not yet measured
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
Hanahan, D., & Weinberg, R. A. (2000) · Cell · doi:10.1016/s0092-8674(00)81683-9 · Cited by 29,219
Apoptosis in the Pathogenesis and Treatment of Disease
Thompson, C. B. (1995) · Science · doi:10.1126/science.7878464 · Cited by 6,524
Extension of Life-Span by Introduction of Telomerase into Normal Human Cells
Bodnar, A. G., Ouellette, M., Frolkis, M., Holt, S. E., Chiu, C.-P., Morin, G. B., Harley, C. B., Shay, J. W., Lichtsteiner, S., & Wright, W. E. (1998) · Science · doi:10.1126/science.279.5349.349 · Cited by 4,975
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
Mechanisms And Functions Of Cell Death
Ellis, R. E., Yuan, J., & Horvitz, H. R. (1991) · Annual Review of Cell Biology · doi:10.1146/annurev.cb.07.110191.003311 · Cited by 2,088
Tumor spectrum analysis in p53-mutant mice
Jacks, T., Remington, L., Williams, B. O., Schmitt, E. M., Halachmi, S., Bronson, R. T., & Weinberg, R. A. (1994) · Current Biology · doi:10.1016/s0960-9822(00)00002-6 · Cited by 2,051
Kirkwood, T. B. L., & Austad, S. N. (2000) · Nature · doi:10.1038/35041682 · Cited by 1,774
Krtolica, A., Parrinello, S., Lockett, S., Desprez, P.-Y., & Campisi, J. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.211053698 · Cited by 1,730
Self-citationVaux, D. L., & Korsmeyer, S. J. (1999) · Cell · doi:10.1016/s0092-8674(00)80564-4 · Cited by 1,564
p53 mutant mice that display early ageing-associated phenotypes
Tyner, S. D., Venkatachalam, S., Choi, J., Jones, S., Ghebranious, N., Igelmann, H., Lu, X., Soron, G., Cooper, B., Brayton, C., et al. (2002) · Nature · doi:10.1038/415045a · Cited by 1,459 · cited 1×
“Strikingly, it also accelerated aging in some tissues, and modestly decreased the life span (Tyner et al., 2002).”
Background
Research works printed but not linked: 1
- Dimri, G. P., Lee, X., Basile, G., Acosta, M., Scott, G., Roskelley, C., Medrano, E. E., Linskens, M., Rubelj, I., Pereira-Smith, O. M., Peacocke, M., Campisi, J. 1995. A novel biomarker identifies senescent human cells in culture and in aging skin in vivo. Proc. Natl. Acad. Sci. USA 92, 9363-9367.
Cited by
Sorted by citations
Items 201–218 of 218
CARF Regulates Cellular Senescence and Apoptosis through p53-Dependent and -Independent Pathways
Wadhwa, R., Singh, R., Kaul, Z., & Kaul, S. C. (2013) · Humana Press eBooks · doi:10.1007/978-1-62703-456-2_8
and their importance in health biotechnology
Salazar, M. M. (2009) · Dialnet (Universidad de la Rioja)
LoCicero, J., Bierman, A. S., Coleman, A. L., Danis, M., Drach, G. W., Gerson, L. W., Hanson, L. C., Karpman, R. R., Lee, A. G., Parnes, S. M., et al. (2011)
Muehlenbein, M. P. (2010) · Cambridge University Press eBooks · doi:10.1017/cbo9780511781193.033
ROLE OF INSULIN RESISTANCE IN THE DEVELOPMENT OF PREMATURE AGING IN PATIENTS WITH METABOLIC SYNDROME
Chernysheva, E. N., Panova, среди, Т., индустриально, Н., & стран, Р. (2013)
Campisi, J. (2008) · Elsevier eBooks · doi:10.1016/b978-141603703-3.10016-0 · Cited by 1
Self-citationA Telomere-Independent Process?
Sharpless, N. E. (2008)
Helicases and Their Relevance to Aging
Crouch, J. D., Banerjee, T., Awate, S., Bharti, S. K., & Brosh, R. M. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-811353-0.00072-5
Cardiorenal Protection in Diabetes Mellitus
Vashistha, H., Meggs, L. G., & Malhotra, A. (2011) · Springer eBooks · doi:10.1007/978-1-4419-7130-2_26
Anti-Aging Medicine LiteratureWatch
(2003) · Rejuvenation Research · doi:10.1089/109454503769684838
Nicholl, C. G., Wilson, K. J., & D'Souza, S. (2025) · Wiley eBooks · doi:10.1002/9781394397976.ch3
Exploring promising pharmaceutical candidates for antiaging
Nandi, N. K., Lodhi, A., Kumar, D., Lather, V., & Tripathi, P. N. (2025) · Elsevier eBooks · doi:10.1016/b978-0-443-36295-8.00014-6
Same mitochondria, different longevities : what do ants tell us about metabolic ageing ?
Kervella, M. (2023) · theses.fr (ABES) · doi:10.70675/7b57ef70z057dz4435za749zb0c6dcd534e4
Shvedova, M. (2026) · Frontiers in Aging · doi:10.3389/fragi.2026.1776669
Metadata
- Authors
- Campisi, J.
- Affiliations
- Buck Institute for Research on Aging (US)
- Corresponding author
- Campisi, J
- ORCID
- Campisi, J
- Venue
- Experimental Gerontology
- Publisher
- Elsevier BV
- Published
- 2003-01
- Volume
- 38
- Issue
- 1-2
- Pages
- 5-11
- ISSN
- 0531-5565 (ISSN-L)
- OpenAlex
- W1973723400
- Cited by
- 218
- References
- 70
- Citations by year
- 2026: 1 · 2025: 8 · 2024: 5 · 2023: 7 · 2022: 4 · 2021: 8 · 2020: 6 · 2019: 2 · 2018: 8 · 2017: 6 · 2016: 4 · 2015: 5 · 2014: 10 · 2013: 11 · 2012: 11
- FWCI
- 6.17
- Type
- journal article
- Language
- en
- Open access
- green
- www.escholarship.org
- Locations
- Experimental Gerontology (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- U.S. Department of Energy
- Ellison Medical Foundation
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- cellular senescence, apoptosis, aging, antagonistic pleiotropy, age-related diseases, natural selection, evolutionary trade-offs, aging phenotypes
- MeSH terms
- Aged, Aging, Animals, Gene Expression Regulation, Humans, Mammals, Neoplasms, Genes, Tumor Suppressor, Cellular Senescence, Apoptosis, Multifactorial Inheritance
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
