Evidence map›Paper›PMID 28485491›Full record

ArticleThe Journal of physiology2017

In vitro model to study the effects of matrix stiffening on Ca

Elza D van Deel, Aref Najafi, Dulce Fontoura, Erik Valent, Max Goebel, Kim Kardux, Inês Falcão-Pires, Jolanda van der Velden

Open access · hybridAbstract read
In one paragraph

Article in The Journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.0field-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

20 citing papers in PubMed, 27 citations in OpenAlex.

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  7. Use of Proximity Labeling in Cardiovascular Research.JACC. Basic to translational science · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Elza D van DeelDepartment of Physiology, Amsterdam Cardiovascular Sciences, VU University Medical Center, Amsterdam, the Netherlands.ORCID 0000-0001-5548-2631
Aref NajafiDepartment of Physiology, Amsterdam Cardiovascular Sciences, VU University Medical Center, Amsterdam, the Netherlands.
Dulce FontouraDepartment of Surgery and Physiology, Faculty of Medicine, Universidade do Porto, Portugal.
Erik ValentDepartment of Physiology, Amsterdam Cardiovascular Sciences, VU University Medical Center, Amsterdam, the Netherlands.
Max GoebelDepartment of Physiology, Amsterdam Cardiovascular Sciences, VU University Medical Center, Amsterdam, the Netherlands.
Kim KarduxDepartment of Physiology, Amsterdam Cardiovascular Sciences, VU University Medical Center, Amsterdam, the Netherlands.
Inês Falcão-PiresDepartment of Surgery and Physiology, Faculty of Medicine, Universidade do Porto, Portugal.
Jolanda van der VeldenDepartment of Physiology, Amsterdam Cardiovascular Sciences, VU University Medical Center, Amsterdam, the Netherlands.
Amsterdam UMC Location Vrije Universiteit Amsterdam · NLUniversidade do Porto · PTNetherlands Heart Institute · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

key pointsThis paper describes a novel model that allows exploration of matrix-induced cardiomyocyte adaptations independent of the passive effect of matrix rigidity on cardiomyocyte function. Detachment of adult cardiomyocytes from the matrix enables the study of matrix effects on cell shortening, Ca ABSTRACT: Extracellular matrix (ECM) stiffening is a key element of cardiac disease. Increased rigidity of the ECM passively inhibits cardiac contraction, but if and how matrix stiffening also actively alters cardiomyocyte contractility is incompletely understood. In vitro models designed to study cardiomyocyte-matrix interaction lack the possibility to separate passive inhibition by a stiff matrix from active matrix-induced alterations of cardiomyocyte properties. Here we introduce a novel experimental model that allows exploration of cardiomyocyte functional alterations in response to matrix stiffening. Adult rat cardiomyocytes were cultured for 24 h on matrices of tuneable stiffness representing the healthy and the diseased heart and detached from their matrix before functional measurements. We demonstrate that matrix stiffening, independent of passive inhibition, reduces cell shortening and Ca

Indexed as

AnimalsCalciumDiabetes MellitusExtracellular MatrixMaleMyocytes, CardiacMyofibrilsObesityRats, WistarCalciumcardiomyocyte functioncell cultureexperimental modelextracellular matrix

Identifiers

PMID28485491
PMCPMC5509860
OpenAlexW2612428948

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.