Evidence map›Paper›PMID 40588563›Full record

ArticleEMBO molecular medicine2025

Chemical reprogramming ameliorates cellular hallmarks of aging and extends lifespan.

Lucas Schoenfeldt, Patrick T Paine, Sara Picó, Nibrasul H Kamaludeen M, Grace B Phelps, Calida Mrabti, Gabriela Desdín-Micó, María Del Carmen Maza, Kevin Perez, Alejandro Ocampo

Abstract read
In one paragraph

Article in EMBO molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

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  18. Somatic mutation as an explanation for epigenetic aging.bioRxiv : the preprint server for biology · 2023
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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.

Lucas Schoenfeldt *Department of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Vaud, Switzerland.ORCID http://orcid.org/0000-0003-1487-0747
Patrick T Paine *Department of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Vaud, Switzerland.
Sara Picó *Department of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Vaud, Switzerland.
Nibrasul H Kamaludeen MDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Vaud, Switzerland.
Grace B PhelpsDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Vaud, Switzerland.
Calida MrabtiDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Vaud, Switzerland.
Gabriela Desdín-MicóDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Vaud, Switzerland.ORCID http://orcid.org/0000-0001-8136-4145
María Del Carmen MazaDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Vaud, Switzerland.
Kevin PerezDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Vaud, Switzerland. kevin@epiterna.com.ORCID http://orcid.org/0000-0002-1802-185X
Alejandro OcampoDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Vaud, Switzerland. alejandro.ocampo@unil.ch.ORCID http://orcid.org/0000-0002-3731-3647

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The dedifferentiation of somatic cells into a pluripotent state by cellular reprogramming coincides with a reversal of age-associated molecular hallmarks. Although transcription factor induced cellular reprogramming has been shown to ameliorate these aging phenotypes in human cells and extend health and lifespan in mice, translational applications of this approach are still limited. More recently, chemical reprogramming via small molecule cocktails have demonstrated a similar ability to induce pluripotency in vitro, however, its potential impact on aging is unknown. Here, we demonstrated that chemical-induced partial reprogramming can improve key drivers of aging including genomic instability and epigenetic alterations in aged human cells. Moreover, we identified an optimized combination of two reprogramming molecules sufficient to induce the amelioration of additional aging phenotypes including cellular senescence and oxidative stress. Importantly, in vivo application of this two-chemical combination significantly extended C. elegans lifespan and healthspan. Together, these data demonstrate that improvement of key drivers of aging and lifespan extension is possible via chemical-induced partial reprogramming, opening a path towards future translational applications.

Indexed as

AgingCellular ReprogrammingCellular SenescenceLongevityAnimalsCaenorhabditis elegansEpigenesis, GeneticGenomic InstabilityHumansOxidative StressAgingCellular ReprogrammingChemical ReprogrammingEpigeneticsLifespan

Identifiers

PMID40588563
PMCPMC12340157

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.