DNA repair‐deficient premature aging models display accelerated epigenetic age
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Abstract
Several premature aging mouse models have been developed to study aging and identify interventions that can delay age‐related diseases. Yet, it is still unclear whether these models truly recapitulate natural aging. Here, we analyzed DNA methylation in multiple tissues of four previously reported mouse models of premature aging ( Ercc1 , LAKI , Polg , and Xpg ). We estimated DNA methylation (DNAm) age of these samples using the Horvath clock. The most pronounced increase in DNAm age could be observed in Ercc1 mice, a strain which exhibits a deficit in DNA nucleotide excision repair. Similarly, we detected an increase in epigenetic age in fibroblasts isolated from patients with progeroid syndromes associated with mutations in DNA excision repair genes. These findings highlight that mouse models with deficiencies in DNA repair, unlike other premature aging models, display accelerated epigenetic age, suggesting a strong connection between DNA damage and epigenetic dysregulation during aging.
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- Authors
- Perez, K., Parras, A., Picó, S., Rechsteiner, C., Haghani, A., Brooke, R., Mrabti, C., Schoenfeldt, L., Horvath, S., & Ocampo, A.
- Affiliations
- Department of Biomedical Sciences, Faculty of Biology and Medicine University of Lausanne Lausanne Switzerland
- University of Lausanne (CH)
- Altos Labs (US)
- Epigenetic Clock Development Foundation Torrance California USA
- University of California, Los Angeles (US)
- Corresponding author
- Ocampo, Alejandro
- ORCID
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2023-12-22
- Volume
- 23
- Issue
- 2
- Pages
- e14058-e14058
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- PMC
- PMC10861193
- OpenAlex
- W4390144018
- Cited by
- 31
- References
- 47
- Citations by year
- 2026: 12 · 2025: 11 · 2024: 5 · 2023: 2 · 2021: 1
- FWCI
- 2.66
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Aging Cell (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- SERVAL (Université de Lausanne) (submittedVersion, cc-by)
- IRIS (submittedVersion, cc-by)
- Funders
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- premature aging, epigenetic age, DNA methylation, Horvath clock, DNA repair deficiency, nucleotide excision repair, ERCC1, DNA polymerase gamma, XPG, progeroid syndromes, DNA damage, mouse models of aging, fibroblasts
- MeSH terms
- Aging, Animals, DNA, DNA Repair, Humans, Proteins, DNA Methylation, Aging, Premature, Epigenesis, Genetic, Mice
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