Evidence map›Paper›PMID 30304034›Full record

ArticlePloS one2018

Hippo signaling pathway is altered in Duchenne muscular dystrophy.

Gian Luca Vita, Francesca Polito, Rosaria Oteri, Roberto Arrigo, Anna Maria Ciranni, Olimpia Musumeci, Sonia Messina, Carmelo Rodolico, Rosa Maria Di Giorgio, Giuseppe Vita and 1 more

Expression of concernOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 56 citations in OpenAlex.

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  14. Dystrophin missense mutations alter focal adhesion tension and mechanotransduction.Proceedings of the National Academy of Sciences of the United States of America · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Gian Luca VitaNemo Sud Clinical Centre for Neuromuscular Disorders, Messina, Italy.
Francesca PolitoUnit of Neurology and Neuromuscular Diseases, Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
Rosaria OteriUnit of Neurology and Neuromuscular Diseases, Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
Roberto ArrigoUnit of Neurology and Neuromuscular Diseases, Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
Anna Maria CiranniUnit of Neurology and Neuromuscular Diseases, Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
Olimpia MusumeciUnit of Neurology and Neuromuscular Diseases, Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
Sonia MessinaNemo Sud Clinical Centre for Neuromuscular Disorders, Messina, Italy.
Carmelo RodolicoNemo Sud Clinical Centre for Neuromuscular Disorders, Messina, Italy.
Rosa Maria Di GiorgioUnit of Neurology and Neuromuscular Diseases, Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
Giuseppe VitaNemo Sud Clinical Centre for Neuromuscular Disorders, Messina, Italy.ORCID 0000-0002-5204-7826
M'Hammed AguennouzUnit of Neurology and Neuromuscular Diseases, Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
University of Messina · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hippo signaling pathway is considered a key regulator of tissue homeostasis, cell proliferation, apoptosis and it is involved in cancer development. In skeletal muscle, YAP, a downstream target of the Hippo pathway, is an important player in myoblast proliferation, atrophy/hypertrophy regulation, and in mechano-trasduction, transferring mechanical signals into transcriptional responses. We studied components of Hippo pathway in muscle specimens from patients with Duchenne muscular dystrophy (DMD), Becker muscular dystrophy, limb-girdle muscular dystrophy type 2A and type 2B and healthy subjects. Only DMD muscles had decreased YAP1 protein expression, increased LATS1/2 kinase activity, low Survivin mRNA expression and high miR-21 expression. In light of our novel results, a schematic model is postulated: low levels of YOD1 caused by increased inhibition by miR-21 lead to an increase of LATS1/2 activity which in turn augments phosphorylation of YAP. Reduced amount of active YAP, which is also a target of increased miR-21, causes decreased nuclear expression of YAP-mediated target genes. Since it is known that YAP has beneficial roles in promoting tissue repair and regeneration after injury so that its activation may be therapeutically useful, our results suggest that some components of Hippo pathway could become novel therapeutic targets for DMD treatment.

Indexed as

Adaptor Proteins, Signal TransducingAdolescentAdultAnimalsCell Cycle ProteinsChildChild, PreschoolHumansMice, Inbred C57BLMice, TransgenicMicroRNAsMiddle AgedMuscle, SkeletalMuscular Dystrophies, Limb-GirdleMuscular Dystrophy, DuchennePhosphoproteinsAdaptor Proteins, Signal TransducingBIRC5 protein, humanCell Cycle ProteinsMicroRNAsMIRN21 microRNA, humanMIRN21 microRNA, mousePhosphoproteinsProtein Serine-Threonine KinasesRNA, MessengerSurvivinTranscription FactorsYAP1 protein, humanYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID30304034
PMCPMC6179272
OpenAlexW2896681008

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.