Evidence map›Paper›PMID 30389913›Full record

ArticleNature communications2018

Myh10 deficiency leads to defective extracellular matrix remodeling and pulmonary disease.

Hyun-Taek Kim, Wenguang Yin, Young-June Jin, Paolo Panza, Felix Gunawan, Beate Grohmann, Carmen Buettner, Anna M Sokol, Jens Preussner, Stefan Guenther and 10 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.6field-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

30 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
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  6. Characterization of Corneal Defects in ATG7-Deficient Mice.International journal of molecular sciences · 2025
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  12. Review
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  14. Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  15. Article
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  17. Article
  18. Review
  19. Article
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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

20 authors at 4 institutions in 3 countries.

Hyun-Taek KimDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany. hyun-taek.kim@mpi-bn.mpg.de.
Wenguang YinDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.ORCID http://orcid.org/0000-0003-1722-8637
Young-June JinDepartment of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.
Paolo PanzaDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.ORCID http://orcid.org/0000-0002-8702-5504
Felix GunawanDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.ORCID http://orcid.org/0000-0002-5592-9680
Beate GrohmannDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.
Carmen BuettnerDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.
Anna M SokolScientific Service Group of Biomolecular Mass Spectrometry, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.ORCID http://orcid.org/0000-0002-8365-3458
Jens PreussnerECCPS Bioinformatics and Deep Sequencing Platform, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.
Stefan GuentherECCPS Bioinformatics and Deep Sequencing Platform, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.
Sawa KostinScientific Service Group of Morphometry, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.ORCID http://orcid.org/0000-0002-1594-9476
Clemens RuppertBiobank, University of Giessen & Marburg Lung Center (UGLMC), Giessen, 35392, Germany.
Aditya M BhagwatBioinformatics Core, Weill Cornell Medicine - Qatar, Doha, PO 24144, Qatar.
Xuefei MaLaboratory of Molecular Cardiology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20814, USA.
Johannes GraumannScientific Service Group of Biomolecular Mass Spectrometry, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.ORCID http://orcid.org/0000-0002-3015-5850
Mario LoosoECCPS Bioinformatics and Deep Sequencing Platform, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.
Andreas GuentherBiobank, University of Giessen & Marburg Lung Center (UGLMC), Giessen, 35392, Germany.
Robert S AdelsteinLaboratory of Molecular Cardiology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20814, USA.
Stefan OffermannsDepartment of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.
Didier Y R StainierDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany. didier.stainier@mpi-bn.mpg.de.
Max Planck Institute for Heart and Lung Research · DEJustus-Liebig-Universität Gießen · DENational Institutes of Health · USWeill Cornell Medical College in Qatar · QA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Impaired alveolar formation and maintenance are features of many pulmonary diseases that are associated with significant morbidity and mortality. In a forward genetic screen for modulators of mouse lung development, we identified the non-muscle myosin II heavy chain gene, Myh10. Myh10 mutant pups exhibit cyanosis and respiratory distress, and die shortly after birth from differentiation defects in alveolar epithelium and mesenchyme. From omics analyses and follow up studies, we find decreased Thrombospondin expression accompanied with increased matrix metalloproteinase activity in both mutant lungs and cultured mutant fibroblasts, as well as disrupted extracellular matrix (ECM) remodeling. Loss of Myh10 specifically in mesenchymal cells results in ECM deposition defects and alveolar simplification. Notably, MYH10 expression is downregulated in the lung of emphysema patients. Altogether, our findings reveal critical roles for Myh10 in alveologenesis at least in part via the regulation of ECM remodeling, which may contribute to the pathogenesis of emphysema.

Indexed as

Amino Acid SequenceAnimalsDown-RegulationEmphysemaEthylnitrosoureaExtracellular MatrixFemaleLung DiseasesMaleMatrix Metalloproteinase 2MesodermMice, Inbred C57BLMutagenesisMutation, MissenseMyosin Heavy ChainsNonmuscle Myosin Type IIBEthylnitrosoureaMatrix Metalloproteinase 2Myosin Heavy ChainsNonmuscle Myosin Type IIBnonmuscle myosin type IIB heavy chain

Identifiers

PMID30389913
PMCPMC6214918
OpenAlexW2951575982

What OpenQuestion holds

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LicenceCC BY
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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.