Evidence map›Paper›PMID 34944046›Full record

ArticleCells2021

Characterization of Type 1 Angiotensin II Receptor Activation Induced Dual-Specificity MAPK Phosphatase Gene Expression Changes in Rat Vascular Smooth Muscle Cells.

Janka Borbála Gém, Kinga Bernadett Kovács, Laura Szalai, Gyöngyi Szakadáti, Edit Porkoláb, Bence Szalai, Gábor Turu, András Dávid Tóth, Mária Szekeres, László Hunyady and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Direct Vascular Effects of Angiotensin II (A Systematic Short Review).International journal of molecular sciences · 2024
    Pooled it
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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

11 authors at 1 institution in 1 country.

Janka Borbála GémDepartment of Physiology, Faculty of Medicine, Semmelweis University, 1085 Budapest, Hungary.
Kinga Bernadett KovácsDepartment of Physiology, Faculty of Medicine, Semmelweis University, 1085 Budapest, Hungary.
Laura SzalaiDepartment of Physiology, Faculty of Medicine, Semmelweis University, 1085 Budapest, Hungary.ORCID 0000-0002-4780-7624
Gyöngyi SzakadátiDepartment of Physiology, Faculty of Medicine, Semmelweis University, 1085 Budapest, Hungary.
Edit PorkolábDepartment of Physiology, Faculty of Medicine, Semmelweis University, 1085 Budapest, Hungary.
Bence SzalaiDepartment of Physiology, Faculty of Medicine, Semmelweis University, 1085 Budapest, Hungary.
Gábor TuruDepartment of Physiology, Faculty of Medicine, Semmelweis University, 1085 Budapest, Hungary.ORCID 0000-0002-4421-3812
András Dávid TóthDepartment of Physiology, Faculty of Medicine, Semmelweis University, 1085 Budapest, Hungary.ORCID 0000-0003-2746-9370
Mária SzekeresDepartment of Physiology, Faculty of Medicine, Semmelweis University, 1085 Budapest, Hungary.ORCID 0000-0002-6967-1158
László HunyadyDepartment of Physiology, Faculty of Medicine, Semmelweis University, 1085 Budapest, Hungary.
András BallaDepartment of Physiology, Faculty of Medicine, Semmelweis University, 1085 Budapest, Hungary.
Semmelweis University · HU

Funding

Hungarian National Research, Development and Innovation Fund NKFI K116954Hungarian National Research, Development and Innovation Fund NVKP_16-1-2016-0039Hungarian National Research, Development and Innovation Fund VEKOP-2.3.2-16-2016-00002
6 · The paper itself

Abstract

Activation of the type I angiotensin receptor (AT1-R) in vascular smooth muscle cells (VSMCs) plays a crucial role in the regulation of blood pressure; however, it is also responsible for the development of pathological conditions such as vascular remodeling, hypertension and atherosclerosis. Stimulation of the VSMC by angiotensin II (AngII) promotes a broad variety of biological effects, including gene expression changes. In this paper, we have taken an integrated approach in which an analysis of AngII-induced gene expression changes has been combined with the use of small-molecule inhibitors and lentiviral-based gene silencing, to characterize the mechanism of signal transduction in response to AngII stimulation in primary rat VSMCs. We carried out Affymetrix GeneChip experiments to analyze the effects of AngII stimulation on gene expression; several genes, including

Indexed as

Gene Expression Regulation, EnzymologicAngiotensin IIAnimalsCell LineEpidermal Growth FactorErbB ReceptorsKineticsLentivirusMaleMatrix MetalloproteinasesMitogen-Activated Protein Kinase PhosphatasesMuscle, Smooth, VascularMyocytes, Smooth MuscleProtein Kinase InhibitorsRatsRats, WistarAngiotensin IIEpidermal Growth FactorErbB ReceptorsMatrix MetalloproteinasesMitogen-Activated Protein Kinase PhosphatasesProtein Kinase InhibitorsReceptor, Angiotensin, Type 1RNA, Small Interferingangiotensin II (AngII)dual-specificity MAPK phosphatase (DUSP)epidermal growth factor receptor (EGFR)G protein-coupled receptor (GPCR)mitogen-activated protein kinase (MAPK)type 1 angiotensin receptor (AT1-R)vascular smooth muscle cell (VSMC)

Identifiers

PMID34944046
PMCPMC8700539
OpenAlexW4200436618

What OpenQuestion holds

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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.