Evidence map›Paper›PMID 32873862›Full record

ArticleScientific reports2020

Myocardial proteomic profile in pulmonary arterial hypertension.

Mateusz K Hołda, Aneta Stachowicz, Maciej Suski, Dorota Wojtysiak, Natalia Sowińska, Zbigniew Arent, Natalia Palka, Piotr Podolec, Grzegorz Kopeć

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 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
1.5field-weighted citation impact, top 14% 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, 21 citations in OpenAlex.

  1. Article
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  5. Blockage of the adenosine APurinergic signalling · 2024
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  8. Association Between Circulating CD4Journal of cardiovascular translational research · 2023
    Article
  9. Article
  10. Effects of the peripheral CBFrontiers in pharmacology · 2022
    Article
  11. Article
  12. Article
  13. Proteomic analysis of pulmonary arterial hypertension.Therapeutic advances in chronic disease · 2021
    Review
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

9 authors at 3 institutions in 2 countries.

Mateusz K Hołda *HEART - Heart Embryology and Anatomy Research Team, Department of Anatomy, Jagiellonian University Medical College, Kopernika 12, 31-034, Kraków, Poland. mkh@onet.eu.
Aneta Stachowicz *Department of Pharmacology, Jagiellonian University Medical College, Kraków, Poland.
Maciej SuskiDepartment of Pharmacology, Jagiellonian University Medical College, Kraków, Poland.
Dorota WojtysiakDepartment of Animal Genetics, Breeding and Ethology, University of Agriculture in Cracow, Kraków, Poland.
Natalia SowińskaCenter of Experimental and Innovative Medicine, University Center of Veterinary Medicine JU-AU, University of Agriculture in Cracow, Kraków, Poland.
Zbigniew ArentCenter of Experimental and Innovative Medicine, University Center of Veterinary Medicine JU-AU, University of Agriculture in Cracow, Kraków, Poland.
Natalia PalkaDepartment of Cardiac and Vascular Diseases, Jagiellonian University Medical College, Kraków, Poland.
Piotr PodolecDepartment of Cardiac and Vascular Diseases, Jagiellonian University Medical College, Kraków, Poland.
Grzegorz KopećDepartment of Cardiac and Vascular Diseases, Jagiellonian University Medical College, Kraków, Poland.
Jagiellonian University · PLUniversity of Agriculture in Krakow · PLUniversity of Manchester · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a rare, fatal, and incurable disorder. Although advances in the understanding of the PAH pathobiology have been seen in recent years, molecular processes underlying heart remodelling over the course of PAH are still insufficiently understood. Therefore, the aim of this study was to investigate myocardial proteomic profile of rats at different stages of monocrotaline-induced PAH. Samples of left and right ventricle (LV and RV) free wall collected from 32 Wistar rats were subjected to proteomic analysis using an isobaric tag for relative quantitation method. Hemodynamic parameters indicated development of mild elevation of pulmonary artery pressure in the early PAH group (27.00 ± 4.93 mmHg) and severe elevation in the end-stage PAH group (50.50 ± 11.56 mmHg). In early PAH LV myocardium proteins that may be linked to an increase in inflammatory response, apoptosis, glycolytic process and decrease in myocardial structural proteins were differentially expressed compared to controls. During end-stage PAH an increase in proteins associated with apoptosis, fibrosis and cardiomyocyte Ca

Indexed as

AnimalsDisease Models, AnimalGene OntologyHemodynamicsHypertrophy, Right VentricularMaleMyocardiumProtein Interaction MapsProteinsProteomeProteomicsPulmonary Arterial HypertensionRatsRats, WistarVentricular RemodelingProteinsProteome

Identifiers

PMID32873862
PMCPMC7462861
OpenAlexW3082846676

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.