Evidence map›Paper›PMID 37118067›Full record

ArticleNature aging2022

In vivo cyclic induction of the FOXM1 transcription factor delays natural and progeroid aging phenotypes and extends healthspan.

Rui Ribeiro, Joana C Macedo, Madalena Costa, Vladimir Ustiyan, Anastasia V Shindyapina, Alexander Tyshkovskiy, Rita N Gomes, José Pedro Castro, Tanya V Kalin, Francisco Vasques-Nóvoa and 5 more

Abstract read
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In one paragraph

Article in Nature aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 1% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

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  6. Systematic identification of single transcription factor perturbations that drive cellular and tissue rejuvenation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  20. Cell Proliferation and Apoptosis-Key Players in the Lung Aging Process.International journal of molecular sciences · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 3 countries.

Rui RibeiroAging and Aneuploidy Laboratory, i3S - Instituto de Investigação e Inovação em Saúde, IBMC - Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal.ORCID 0000-0003-3759-2399
Joana C MacedoAging and Aneuploidy Laboratory, i3S - Instituto de Investigação e Inovação em Saúde, IBMC - Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal.ORCID 0000-0003-3578-9120
Madalena CostaAnatomy Department, Unit for Multidisciplinary Biomedical Research, ICBAS - Instituto de Ciências Biomédicas de Abel Salazar, Universidade do Porto, Porto, Portugal.
Vladimir UstiyanCenter for Lung Regenerative Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Anastasia V ShindyapinaDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Alexander TyshkovskiyDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-6215-190X
Rita N GomesINEB - Instituto Nacional de Engenharia Biomédica, i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.
José Pedro CastroAging and Aneuploidy Laboratory, i3S - Instituto de Investigação e Inovação em Saúde, IBMC - Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal.ORCID 0000-0002-2627-5331
Tanya V KalinDivision of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.ORCID 0000-0002-8545-8277
Francisco Vasques-NóvoaINEB - Instituto Nacional de Engenharia Biomédica, i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.
Diana S NascimentoINEB - Instituto Nacional de Engenharia Biomédica, i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.ORCID 0000-0001-6402-4245
Sergey E DmitrievBelozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia.ORCID 0000-0002-1774-8475
Vadim N GladyshevDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-0372-7016
Vladimir V KalinichenkoCenter for Lung Regenerative Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.ORCID 0000-0003-3438-2660
Elsa LogarinhoAging and Aneuploidy Laboratory, i3S - Instituto de Investigação e Inovação em Saúde, IBMC - Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal. elsa.logarinho@ibmc.up.pt.ORCID 0000-0002-8741-0744
Universidade do Porto · PTBrigham and Women's Hospital · USCincinnati Children's Hospital Medical Center · USi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto · PTLomonosov Moscow State University · RU

Funding

Role of lung endothelial cells during fibrotic lung remodeling.R01HL158659 · NHLBI · UNIVERSITY OF ARIZONA · PI KALIN, TANYA · 2021 to 2024
$2.2M
Targeting Foxm1 in pulmonary fibrosisR01HL132849 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI KALIN, TANYA · 2016 to 2019
$1.5M
NHLBI NIH HHS R01 HL132849NHLBI NIH HHS R01 HL158659
6 · The paper itself

Abstract

The FOXM1 transcription factor exhibits pleiotropic C-terminal transcriptional and N-terminal non-transcriptional functions in various biological processes critical for cellular homeostasis. We previously found that FOXM1 repression during cellular aging underlies the senescence phenotypes, which were vastly restored by overexpressing transcriptionally active FOXM1. Yet, it remains unknown whether increased expression of FOXM1 can delay organismal aging. Here, we show that in vivo cyclic induction of an N-terminal truncated FOXM1 transgene on progeroid and naturally aged mice offsets aging-associated repression of full-length endogenous Foxm1, reinstating both transcriptional and non-transcriptional functions. This translated into mitigation of several cellular aging hallmarks, as well as molecular and histopathological progeroid features of the short-lived Hutchison-Gilford progeria mouse model, significantly extending its lifespan. FOXM1 transgene induction also reinstated endogenous Foxm1 levels in naturally aged mice, delaying aging phenotypes while extending their lifespan. Thus, we disclose that FOXM1 genetic rewiring can delay senescence-associated progeroid and natural aging pathologies.

Indexed as

AgingTranscription FactorsAnimalsCellular SenescenceForkhead Box Protein M1Gene Expression RegulationMicePhenotypeForkhead Box Protein M1Foxm1 protein, mouseTranscription Factors

Identifiers

PMID37118067
OpenAlexW4229002207

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.