Evidence map›Paper›PMID 31980934›Full record

ArticleBasic research in cardiology2020

FHL-1 is not involved in pressure overload-induced maladaptive right ventricular remodeling and dysfunction.

Christine Veith, Dariusch Neghabian, Himal Luitel, Jochen Wilhelm, Bakytbek Egemnazarov, Caja Muntanjohl, Jan-Hendrik Fischer, Bhola Kumar Dahal, Ralph Theo Schermuly, Hossein Ardeschir Ghofrani and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Basic research in cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.2field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

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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

15 authors at 5 institutions in 2 countries.

Christine VeithMember of the German Center for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Aulweg 130, 35392, Giessen, Germany.
Dariusch NeghabianMember of the German Center for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Aulweg 130, 35392, Giessen, Germany.
Himal LuitelMember of the German Center for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Aulweg 130, 35392, Giessen, Germany.
Jochen WilhelmMember of the German Center for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Aulweg 130, 35392, Giessen, Germany.
Bakytbek EgemnazarovLudwig Boltzmann Institute for Lung Vascular Research, Medical University of Graz, Neue Stiftingtalstrasse 6/VI, 8010, Graz, Austria.
Caja MuntanjohlMember of the German Center for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Aulweg 130, 35392, Giessen, Germany.
Jan-Hendrik FischerMember of the German Center for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Aulweg 130, 35392, Giessen, Germany.
Bhola Kumar DahalMember of the German Center for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Aulweg 130, 35392, Giessen, Germany.
Ralph Theo SchermulyMember of the German Center for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Aulweg 130, 35392, Giessen, Germany.
Hossein Ardeschir GhofraniMember of the German Center for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Aulweg 130, 35392, Giessen, Germany.
Friedrich GrimmingerMember of the German Center for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Aulweg 130, 35392, Giessen, Germany.
Ludger FinkMember of the German Center for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Aulweg 130, 35392, Giessen, Germany.
Grazyna KwapiszewskaLudwig Boltzmann Institute for Lung Vascular Research, Medical University of Graz, Neue Stiftingtalstrasse 6/VI, 8010, Graz, Austria. grazyna.kwapiszewska@lvr.lbg.ac.at.
Norbert WeissmannMember of the German Center for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Aulweg 130, 35392, Giessen, Germany. Norbert.Weissmann@innere.med.uni-giessen.de.
Akylbek SydykovMember of the German Center for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Aulweg 130, 35392, Giessen, Germany. Akylbek.Sydykov@innere.med.uni-giessen.de.
German Center for Lung Research · DEJustus-Liebig-Universität Gießen · DEUniversities of Giessen and Marburg Lung Center · DELudwig Boltzmann Institute for Lung Vascular Research · ATMedical University of Graz · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsThe cytoskeletal signaling protein four and-a-half LIM domains 1 (FHL-1) has recently been identified as a novel key player in pulmonary hypertension as well as in left heart diseases. In this regard, FHL-1 has been implicated in dysregulated hypertrophic signaling in pulmonary arterial smooth muscle cells leading to pulmonary hypertension. In mice, FHL-1-deficiency (FHL-1 METHODS AND

resultsWe investigated FHL-1 expression in C57Bl/6 mice subjected to chronic biomechanical stress and found it to be enhanced in the right ventricle (RV). Next, we subjected FHL-1

conclusionFHL-1 pathway is not involved in the control of adverse remodeling in the pressure overloaded RV.

Indexed as

Ventricular Function, RightVentricular RemodelingAnimalsCalcium-Binding ProteinsDisease Models, AnimalFibrosisHeart VentriclesHypertrophy, Right VentricularIntracellular Signaling Peptides and ProteinsLIM Domain ProteinsMaleMice, Inbred C57BLMice, KnockoutMuscle ProteinsNatriuretic PeptidesPhospholambanCalcium-Binding ProteinsFhl1 protein, mouseIntracellular Signaling Peptides and ProteinsLIM Domain ProteinsMuscle ProteinsNatriuretic PeptidesPhospholambanryanodine receptor 2. mouseRyanodine Receptor Calcium Release ChannelCytoskeletal proteinsFour and-a-half LIM domain 1 proteinPressure overloadPulmonary arterial bandingRight ventricular hypertrophy

Identifiers

PMID31980934
PMCPMC6981327
OpenAlexW3002573205

What OpenQuestion holds

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LicenceCC BY
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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.