Evidence map›Paper›PMID 32755011›Full record

ArticleAging cell2020

Inhibition of Cdc42 activity extends lifespan and decreases circulating inflammatory cytokines in aged female C57BL/6 mice.

Maria Carolina Florian, Hanna Leins, Michael Gobs, Yang Han, Gina Marka, Karin Soller, Angelika Vollmer, Vadim Sakk, Kalpana J Nattamai, Ahmad Rayes and 6 more

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 66 citations in OpenAlex.

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  12. Immunosenescence: signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2025
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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

16 authors at 3 institutions in 3 countries.

Maria Carolina FlorianProgram of Regenerative Medicine, IDIBELL, Barcelona, Spain.ORCID 0000-0002-5791-1310
Hanna LeinsInstitute of Molecular Medicine and Stem Cell Aging, Ulm University, Ulm, Germany.
Michael GobsHelmholtz-Institute for Biomedical Engineering, Stem Cell Biology and Cellular Engineering, RWTH Aachen University Medical School, Aachen, Germany.
Yang HanHelmholtz-Institute for Biomedical Engineering, Stem Cell Biology and Cellular Engineering, RWTH Aachen University Medical School, Aachen, Germany.
Gina MarkaInstitute of Molecular Medicine and Stem Cell Aging, Ulm University, Ulm, Germany.
Karin SollerInstitute of Molecular Medicine and Stem Cell Aging, Ulm University, Ulm, Germany.
Angelika VollmerInstitute of Molecular Medicine and Stem Cell Aging, Ulm University, Ulm, Germany.
Vadim SakkInstitute of Molecular Medicine and Stem Cell Aging, Ulm University, Ulm, Germany.
Kalpana J NattamaiDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA.
Ahmad RayesDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA.
Xueheng ZhaoDivision of Pathology, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA.
Kenneth SetchellDivision of Pathology, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA.
Medhanie MulawInstitute of Experimental Cancer Research, Medical Faculty, University of Ulm, Ulm, Germany.
Wolfgang WagnerHelmholtz-Institute for Biomedical Engineering, Stem Cell Biology and Cellular Engineering, RWTH Aachen University Medical School, Aachen, Germany.ORCID 0000-0002-1971-3217
Yi ZhengDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA.
Hartmut GeigerInstitute of Molecular Medicine and Stem Cell Aging, Ulm University, Ulm, Germany.
Universität Ulm · DECincinnati Children's Hospital Medical Center · USRWTH Aachen University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cdc42 is a small RhoGTPase regulating multiple functions in eukaryotic cells. The activity of Cdc42 is significantly elevated in several tissues of aged mice, while the Cdc42 gain-of-activity mouse model presents with a premature aging-like phenotype and with decreased lifespan. These data suggest a causal connection between elevated activity of Cdc42, aging, and reduced lifespan. Here, we demonstrate that systemic treatment of aged (75-week-old) female C57BL/6 mice with a Cdc42 activity-specific inhibitor (CASIN) for 4 consecutive days significantly extends average and maximum lifespan. Moreover, aged CASIN-treated animals displayed a youthful level of the aging-associated cytokines IL-1β, IL-1α, and INFγ in serum and a significantly younger epigenetic clock as based on DNA methylation levels in blood cells. Overall, our data show that systemic administration of CASIN to reduce Cdc42 activity in aged mice extends murine lifespan.

Indexed as

AgingAnimalscdc42 GTP-Binding ProteinCytokinesDrosophila ProteinsFemaleIntegrin alpha ChainsLongevityMiceMice, Inbred C57BLcdc42 GTP-Binding ProteinCDC42 protein, humanCytokinesDrosophila Proteinsif protein, DrosophilaIntegrin alpha ChainsagingCdc42epigenetic clockinflammaginginterferon gammalifespan

Identifiers

PMID32755011
PMCPMC7511875
OpenAlexW3047123911

What OpenQuestion 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 OpenQuestion graph.