Evidence map›Paper›PMID 36550158›Full record

ArticleNature communications2022

Actin-microtubule cytoskeletal interplay mediated by MRTF-A/SRF signaling promotes dilated cardiomyopathy caused by LMNA mutations.

Caroline Le Dour, Maria Chatzifrangkeskou, Coline Macquart, Maria M Magiera, Cécile Peccate, Charlène Jouve, Laura Virtanen, Tiina Heliö, Katriina Aalto-Setälä, Silvia Crasto and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.2field-weighted citation impact, top 4% 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, 56 citations in OpenAlex.

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  20. Dysfunctional cardiomyocyte signalling and heart disease.Current opinion in cell biology · 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

19 authors at 7 institutions in 4 countries.

Caroline Le Dour *Centre de recherche en Myologie, U974 SU-INSERM, 75013, Paris, France.ORCID 0000-0001-8647-3252
Maria Chatzifrangkeskou *Centre de recherche en Myologie, U974 SU-INSERM, 75013, Paris, France.
Coline Macquart *Centre de recherche en Myologie, U974 SU-INSERM, 75013, Paris, France.
Maria M MagieraInstitut Curie, Université PSL, CNRS UMR3348, 91401, Orsay, France.ORCID 0000-0003-4847-3053
Cécile PeccateCentre de recherche en Myologie, U974 SU-INSERM, 75013, Paris, France.
Charlène JouveUniversité de Paris, Paris Cardiovascular Research Center PARCC, INSERM, 75015, Paris, France.ORCID 0000-0002-5792-4621
Laura VirtanenInstitute of Biomedicine and FICAN West Cancer Centre, University of Turku, 20520, Turku, Finland.
Tiina HeliöHeart and Lung Centre, Helsinki University Central Hospital, University of Helsinki, 00290, Helsinki, Finland.
Katriina Aalto-SetäläFaculty of Medicine and Health Technology and BioMediTech Institute, Tampere University, 33520, Tampere, Finland.ORCID 0000-0003-0334-2172
Silvia CrastoInstitute of Genetic and Biomedical Research (IRGB), UOS of Milan, National Research Council of Italy, Milan, Italy.
Bruno CadotCentre de recherche en Myologie, U974 SU-INSERM, 75013, Paris, France.
Déborah CardosoCentre de recherche en Myologie, U974 SU-INSERM, 75013, Paris, France.
Nathalie MougenotSorbonne Université, INSERM, UMS28 Phénotypage du petit animal, Paris, 75013, France.
Daniel AdesseFundação Oswaldo Cruz, Instituto Oswaldo Cruz, Laboratório de Biologia Estrutural, Rio de Janeiro, Brasil.ORCID 0000-0002-7421-9510
Elisa Di PasqualeInstitute of Genetic and Biomedical Research (IRGB), UOS of Milan, National Research Council of Italy, Milan, Italy.ORCID 0000-0003-2373-5635
Jean-Sébastien HulotUniversité de Paris, Paris Cardiovascular Research Center PARCC, INSERM, 75015, Paris, France.
Pekka TaimenInstitute of Biomedicine and FICAN West Cancer Centre, University of Turku, 20520, Turku, Finland.ORCID 0000-0001-8849-4604
Carsten JankeInstitut Curie, Université PSL, CNRS UMR3348, 91401, Orsay, France.ORCID 0000-0001-7053-2000
Antoine MuchirCentre de recherche en Myologie, U974 SU-INSERM, 75013, Paris, France. a.muchir@institut-myologie.org.ORCID 0000-0002-4780-9275
Inserm · FRCentre National de la Recherche Scientifique · FRHumanitas University · ITUniversity of Turku · FIFundação Oswaldo Cruz · BRTampere University · FIUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in the lamin A/C gene (LMNA) cause dilated cardiomyopathy associated with increased activity of ERK1/2 in the heart. We recently showed that ERK1/2 phosphorylates cofilin-1 on threonine 25 (phospho(T25)-cofilin-1) that in turn disassembles the actin cytoskeleton. Here, we show that in muscle cells carrying a cardiomyopathy-causing LMNA mutation, phospho(T25)-cofilin-1 binds to myocardin-related transcription factor A (MRTF-A) in the cytoplasm, thus preventing the stimulation of serum response factor (SRF) in the nucleus. Inhibiting the MRTF-A/SRF axis leads to decreased α-tubulin acetylation by reducing the expression of ATAT1 gene encoding α-tubulin acetyltransferase 1. Hence, tubulin acetylation is decreased in cardiomyocytes derived from male patients with LMNA mutations and in heart and isolated cardiomyocytes from Lmna

Indexed as

Cardiomyopathy, DilatedActin Depolymerizing FactorsActinsAnimalsConnexin 43Intermediate Filament ProteinsLamin Type AMaleMiceMice, KnockoutMicrotubulesMutationMyocardinMyocytes, CardiacSerum Response FactorTubulinActin Depolymerizing FactorsActinsConnexin 43Intermediate Filament ProteinsLamin Type AMyocardinSerum Response FactorTubulin

Identifiers

PMID36550158
PMCPMC9780334
OpenAlexW4312192987

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.