The DOI matches its Crossref record; 98 of the 98 references it cites were found in a registry or an index.
Impact of genomic damage and ageing on stem cell function
Open accessAbstract
Impairment of stem cell function contributes to the progressive deterioration of tissue maintenance and repair with ageing. Evidence is mounting that age-dependent accumulation of DNA damage in both stem cells and cells that comprise the stem cell microenvironment are partly responsible for stem cell dysfunction with ageing. Here, we review the impact of the various types of DNA damage that accumulate with ageing on stem cell functionality, as well as the development of cancer. We discuss DNA-damage-induced cell intrinsic and extrinsic alterations that influence these processes, and review recent advances in understanding systemic adjustments to DNA damage and how they affect stem cells.
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
“Quite often, defects in DNA repair systems of stem cells accelerate the accumulation of genome instability in lineage-primed progenitor cells during aging [46].”
From Ultraviolet Radiation‐Induced Skin Aging: The Role of DNA Damage and Oxidative Stress in Epidermal Stem Cell Damage Mediated Skin Aging (2016) · cites this paper as [46]
In the citing paper
“Although not a bona fide DNA repair gene, defects in ATM lead to accumulation of genomic damage and premature exhaustion of the stem cell pool in various tissues, including the skin [46].”
From Ultraviolet Radiation‐Induced Skin Aging: The Role of DNA Damage and Oxidative Stress in Epidermal Stem Cell Damage Mediated Skin Aging (2016) · cites this paper as [46]
In the citing paper
“These observations suggest that DDR pathways, evolved to safeguard genomic integrity and maximize survival of the organism13,44–46, may show reduced activity in stem cells with age.”
From Stem cell aging: mechanisms, regulators and therapeutic opportunities (2014) · cites this paper as [46]
In the citing paper
“Some studies suggest that the ensuing loss of homeostasis in aging tissues might further create a microenvironment that favors the selection of stem cells with higher self-renewal but also neoplastic potentials46.”
From Stem cell aging: mechanisms, regulators and therapeutic opportunities (2014) · cites this paper as [46]
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
Hallmarks of Cancer: The Next Generation
Hanahan, D., & Weinberg, R. A. (2011) · Cell · doi:10.1016/j.cell.2011.02.013 · Cited by 66,590
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
A C. elegans mutant that lives twice as long as wild type
Kenyon, C., Chang, J., Gensch, E., Rudner, A., & Tabtiang, R. (1993) · Nature · doi:10.1038/366461a0 · Cited by 3,387
Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas
Xue, W., Zender, L., Miething, C., Dickins, R. A., Hernando, E., Krizhanovsky, V., Cordon-Cardo, C., & Lowe, S. W. (2007) · Nature · doi:10.1038/nature05529 · Cited by 2,473
Rejuvenation of aged progenitor cells by exposure to a young systemic environment
Conboy, I. M., Conboy, M. J., Wagers, A. J., Girma, E. R., Weissman, I. L., & Rando, T. A. (2005) · Nature · doi:10.1038/nature03260 · Cited by 2,287
IGF-1 receptor regulates lifespan and resistance to oxidative stress in mice
Holzenberger, M., Dupont, J., Ducos, B., Leneuve, P., Géloën, A., Even, P. C., Cervera, P., & Le Bouc, Y. (2003) · Nature · doi:10.1038/nature01298 · Cited by 2,109
Causes and consequences of replication stress
Zeman, M. K., & Cimprich, K. A. (2014) · Nature Cell Biology · doi:10.1038/ncb2897 · Cited by 2,079
Senescence of Activated Stellate Cells Limits Liver Fibrosis
Krizhanovsky, V., Yon, M., Dickins, R. A., Hearn, S., Simon, J., Miething, C., Yee, H., Zender, L., & Lowe, S. W. (2008) · Cell · doi:10.1016/j.cell.2008.09.015 · Cited by 2,027
Snippert, H. J., van der Flier, L. G., Sato, T., van Es, J. H., van den Born, M., Kroon-Veenboer, C., Barker, N., Klein, A. M., van Rheenen, J., Simons, B. D., et al. (2010) · Cell · doi:10.1016/j.cell.2010.09.016 · Cited by 1,951
ATR: an essential regulator of genome integrity
Cimprich, K. A., & Cortez, D. (2008) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2450 · Cited by 1,798
Flagged first, then by citations
Research works printed but not linked: 1
- Krishnamurthy, J. et al. Ink4a/Arf expression is a biomarker of aging. J. Clin. Invest. 114, 1299–1307 (2004). · DOI · Paper page
Cited by
Sorted by citations
Inflammation, fracture and bone repair
Loi, F., Córdova, L. A., Pajarinen, J., Lin, T., Yao, Z., & Goodman, S. B. (2016) · Bone · doi:10.1016/j.bone.2016.02.020 · Cited by 1,339
“Cellular and molecular characterization of non-union tissues has shown that senescent MSCs exhibit a reduced capacity to differentiate into mature, functional osteoblasts [148,149].”
BackgroundMesenchymal stem cell-macrophage crosstalk and bone healing
Pajarinen, J., Lin, T., Gibon, E., Kohno, Y., Maruyama, M., Nathan, K., Lu, L. Y., Yao, Z., & Goodman, S. B. (2018) · Biomaterials · doi:10.1016/j.biomaterials.2017.12.025 · Cited by 1,031
“overexpression of p53, p21, BAX or MYC genes, among other changes [72-75].”
BackgroundMechanisms of maladaptive repair after AKI leading to accelerated kidney ageing and CKD
Ferenbach, D. A., & Bonventre, J. V. (2015) · Nature Reviews Nephrology · doi:10.1038/nrneph.2015.3 · Cited by 892
Stem cell aging: mechanisms, regulators and therapeutic opportunities
Oh, J., Lee, Y. D., & Wagers, A. J. (2014) · Nature Medicine · doi:10.1038/nm.3651 · Cited by 796
The effects of aging in the hippocampus and cognitive decline
Bettio, L. E. B., Rajendran, L., & Gil‐Mohapel, J. (2017) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2017.04.030 · Cited by 700
“Another possibility is that depletion of the NSC pool could be a consequence of an increase in the number of stem cells becoming senescent due to telomeric attrition and/or DNA damage that accumulates with aging (Behrens et al., 2014).”
Metadata
- Authors
- Behrens, A., van Deursen, J. M., Rudolph, K. L., & Schumacher, B.
- Affiliations
- King's College London (GB)
- Leibniz Institute on Aging - Fritz Lipmann Institute (FLI) (DE)
- University of Cologne (DE)
- Corresponding author
- Behrens, Axel
- Rudolph, K. Lenhard
- Schumacher, Björn
- Venue
- Nature Cell Biology
- Published
- 2014-02-28
- Volume
- 16
- Issue
- 3
- Pages
- 201-207
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- PMC
- PMC4214082
- OpenAlex
- W2054525725
- Cited by
- 207
- References
- 98
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 11 · 2023: 12 · 2022: 10 · 2021: 17 · 2020: 19 · 2019: 27 · 2018: 13 · 2017: 18 · 2016: 20 · 2015: 32 · 2014: 13
- FWCI
- 3.24
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Kölner Universitäts PublikationsServer (Universität zu Köln) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Informationszentrum Lebenswissenschaften (ZB MED) (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Funders
- Cancer Research UK (15679)
- National Cancer Institute (R01CA126828)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- genomic instability, aging, stem cell function, DNA damage, stem cell niche, tissue maintenance, tissue repair, carcinogenesis
- MeSH terms
- Aneuploidy, Animals, Cells, Cultured, DNA Damage, DNA Repair, Humans, Neoplasms, Genome, Human, Cellular Senescence, Adult Stem Cells
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
