Evidence map›Paper›PMID 38984541›Full record

ArticleDevelopment (Cambridge, England)2024

Mechanical forces remodel the cardiac extracellular matrix during zebrafish development.

Alessandra Gentile, Marga Albu, Yanli Xu, Newsha Mortazavi, Agatha Ribeiro da Silva, Didier Y R Stainier, Felix Gunawan

Abstract read
In one paragraph

Article in Development (Cambridge, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
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  6. Article
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

7 authors.

Alessandra GentileDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim 61231, Germany.ORCID 0000-0002-5423-7295
Marga AlbuDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim 61231, Germany.ORCID 0009-0004-9409-8762
Yanli XuDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim 61231, Germany.ORCID 0009-0006-4945-6334
Newsha MortazaviInstitute of Cell Biology, Faculty of Medicine, University of Münster, Münster 48149, Germany.ORCID 0000-0003-0958-3479
Agatha Ribeiro da SilvaDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim 61231, Germany.ORCID 0009-0002-8756-1734
Didier Y R StainierDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim 61231, Germany.ORCID 0000-0002-0382-0026
Felix GunawanInstitute of Cell Biology, Faculty of Medicine, University of Münster, Münster 48149, Germany.ORCID 0000-0002-5592-9680

Funding

Deutsche Forschungsgemeinschaft SFB1348B12European Research Council AdG 694455-ZMODMax Planck SocietyUniversity of Münster I-GU122208Westfälische Wilhelms-Universität Münster I-GU122208
6 · The paper itself

Abstract

The cardiac extracellular matrix (cECM) is fundamental for organ morphogenesis and maturation, during which time it undergoes remodeling, yet little is known about whether mechanical forces generated by the heartbeat regulate this remodeling process. Using zebrafish as a model and focusing on stages when cardiac valves and trabeculae form, we found that altering cardiac contraction impairs cECM remodeling. Longitudinal volumetric quantifications in wild-type animals revealed region-specific dynamics: cECM volume decreases in the atrium but not in the ventricle or atrioventricular canal. Reducing cardiac contraction resulted in opposite effects on the ventricular and atrial ECM, whereas increasing the heart rate affected the ventricular ECM but had no effect on the atrial ECM, together indicating that mechanical forces regulate the cECM in a chamber-specific manner. Among the ECM remodelers highly expressed during cardiac morphogenesis, we found one that was upregulated in non-contractile hearts, namely tissue inhibitor of matrix metalloproteinase 2 (timp2). Loss- and gain-of-function analyses of timp2 revealed its crucial role in cECM remodeling. Altogether, our results indicate that mechanical forces control cECM remodeling in part through timp2 downregulation.

Indexed as

Extracellular MatrixHeartTissue Inhibitor of Metalloproteinase-2ZebrafishAnimalsBiomechanical PhenomenaGene Expression Regulation, DevelopmentalHeart AtriaHeart VentriclesMorphogenesisMyocardial ContractionMyocardiumZebrafish ProteinsTissue Inhibitor of Metalloproteinase-2Zebrafish ProteinsBiomechanical forcesCardiac developmentCardiac ECM remodelingZebrafish cardiogenesis

Identifiers

PMID38984541
PMCPMC11266798

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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.