Evidence map›Paper›PMID 42875585›Full record

ArticleNature aging2026

Transcriptomic reprogramming screen identifies SRSF1 as a regulator of aging.

Alexandru M Plesa, Sascha Jung, Helen H Wang, Fawad Omar, Michael Shadpour, David Choy Buentello, Maria C Perez-Matos, Naftali Horwitz, George Cai, Zhen Kai Ngian and 5 more

Abstract read
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In one paragraph

Article in Nature aging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Alexandru M Plesa *Wyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA, USA.ORCID http://orcid.org/0000-0002-0414-4285
Sascha Jung *Computational Biology Group, CIC bioGUNE-BRTA (Basque Research and Technology Alliance), Bizkaia Technology Park, Derio, Spain.
Helen H WangWyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA, USA.ORCID http://orcid.org/0000-0002-5743-2176
Fawad OmarWyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA, USA.
Michael ShadpourWyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA, USA.
David Choy BuentelloDepartment of Genetics, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0002-8076-4005
Maria C Perez-MatosDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.ORCID http://orcid.org/0000-0002-2841-9810
Naftali HorwitzPaul F. Glenn Center for Biology of Aging Research at Harvard Medical School, Boston, MA, USA.
George CaiWyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA, USA.
Zhen Kai NgianDepartment of Genetics, Harvard Medical School, Boston, MA, USA.
Carol MagalhaesWyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA, USA.
Amy J WagersPaul F. Glenn Center for Biology of Aging Research at Harvard Medical School, Boston, MA, USA.
William B MairDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.ORCID http://orcid.org/0000-0002-0661-1342
Antonio Del SolComputational Biology Group, CIC bioGUNE-BRTA (Basque Research and Technology Alliance), Bizkaia Technology Park, Derio, Spain. antonio.delsol@uni.lu.ORCID http://orcid.org/0000-0002-9926-617X
George M ChurchWyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA, USA. gchurch@genetics.med.harvard.edu.ORCID http://orcid.org/0000-0001-6232-9969

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is characterized by progressive functional decline accompanied by distinct transcriptomic and epigenetic alterations. Although partial reprogramming via Yamanaka factors can reverse these signatures and improve cell function, toxicity and efficacy concerns limit their in vivo application, necessitating alternative geroprotective interventions. Here we develop an interpretable transcriptomic age predictor in human fibroblasts and perform a cDNA overexpression screen to identify factors that reprogram aged transcriptomes toward youthful states. This screen identifies the RNA-processing and splicing factor SRSF1 as a regulator of cellular aging that produces robust youthful transcriptional signatures without loss of cellular identity. In vitro, SRSF1 induction restores youthful phenotypes by reducing senescence, proteostatic stress and inflammatory signaling. In aged mice, inducible SRSF1 expression reduces frailty progression by 44% and is associated with a 14% extension of median lifespan (n = 9-10 per group). Our findings establish SRSF1 as a conserved regulator of aging and a promising geroprotective target.

Indexed as

AgingCellular ReprogrammingSerine-Arginine Splicing FactorsTranscriptomeAnimalsCellular SenescenceFibroblastsHumansLongevityMiceSerine-Arginine Splicing FactorsSRSF1 protein, humanSrsf1 protein, mouse

Identifiers

PMID42875585

What OpenQuestion holds

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Registered trials

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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.