Evidence map›Paper›PMID 38140713›Full record

ArticleAging cell2024

DNA repair-deficient premature aging models display accelerated epigenetic age.

Kevin Perez, Alberto Parras, Sara Picó, Cheyenne Rechsteiner, Amin Haghani, Robert Brooke, Calida Mrabti, Lucas Schoenfeldt, Steve Horvath, Alejandro Ocampo

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.9field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 20 citations in OpenAlex.

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  17. Loss of H3K9 trimethylation leads to premature aging.bioRxiv : the preprint server for biology · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 3 countries.

Kevin PerezDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland.
Alberto ParrasDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland.
Sara PicóDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland.
Cheyenne RechsteinerDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland.
Amin HaghaniAltos Labs, San Diego, California, USA.
Robert BrookeEpigenetic Clock Development Foundation, Torrance, California, USA.
Calida MrabtiDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland.
Lucas SchoenfeldtDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland.
Steve HorvathAltos Labs, San Diego, California, USA.ORCID 0000-0002-4110-3589
Alejandro OcampoDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland.ORCID 0000-0002-3731-3647
Electronic Product Services (Czechia) · CZUniversity of Lausanne · CHAltos LabsEpigenetix (United States) · USUniversity of California, Los Angeles · US

Funding

Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
6 · The paper itself

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.

Indexed as

Aging, PrematureAgingAnimalsDNADNA MethylationDNA RepairEpigenesis, GeneticHumansMiceProteinsDNAProteinsaccelerated agingDNA damageepigenetic clockmethylationprogeria

Identifiers

PMID38140713
PMCPMC10861193
OpenAlexW4390144018

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.