Evidence map›Paper›PMID 29311569›Full record

ArticleScientific reports2018

Hepatic dysfunction and thrombocytopenia induced by excess sFlt1 in mice lacking endothelial nitric oxide synthase.

Yuji Oe, Mieko Ko, Tomofumi Fushima, Emiko Sato, S Ananth Karumanchi, Hiroshi Sato, Junichi Sugawara, Sadayoshi Ito, Nobuyuki Takahashi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.6field-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

21 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  10. Genetic Background of Fetal Growth Restriction.International journal of molecular sciences · 2021
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  19. Non-obstetric complications in preeclampsia.Przeglad menopauzalny = Menopause review · 2019
    Review
  20. 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

9 authors at 3 institutions in 2 countries.

Yuji OeDivision of Feto-Maternal Medical Science, Department of Community Medical Support, Tohoku Medical Megabank Organization, Tohoku University, Sendai, 980-8574, Japan.
Mieko KoDivision of Clinical Pharmacology and Therapeutics, Tohoku University Graduate School of Pharmaceutical Sciences & Faculty of Pharmaceutical Sciences, Sendai, 980-8578, Japan.
Tomofumi FushimaDivision of Clinical Pharmacology and Therapeutics, Tohoku University Graduate School of Pharmaceutical Sciences & Faculty of Pharmaceutical Sciences, Sendai, 980-8578, Japan.
Emiko SatoDivision of Clinical Pharmacology and Therapeutics, Tohoku University Graduate School of Pharmaceutical Sciences & Faculty of Pharmaceutical Sciences, Sendai, 980-8578, Japan.
S Ananth KarumanchiDepartment of Medicine and Center for Vascular Biology Research, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02215, USA.
Hiroshi SatoDivision of Clinical Pharmacology and Therapeutics, Tohoku University Graduate School of Pharmaceutical Sciences & Faculty of Pharmaceutical Sciences, Sendai, 980-8578, Japan.
Junichi SugawaraDivision of Feto-Maternal Medical Science, Department of Community Medical Support, Tohoku Medical Megabank Organization, Tohoku University, Sendai, 980-8574, Japan.
Sadayoshi ItoDivision of Nephrology, Endocrinology, and Vascular Medicine, Tohoku University Graduate School of Medicine, Sendai, 980-8574, Japan.
Nobuyuki TakahashiDivision of Clinical Pharmacology and Therapeutics, Tohoku University Graduate School of Pharmaceutical Sciences & Faculty of Pharmaceutical Sciences, Sendai, 980-8578, Japan. ntakaha@m.tohoku.ac.jp.
Tohoku University · JPTohoku Medical Megabank Organization · JPBeth Israel Deaconess Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver dysfunction is a major problem in patients with severe preeclampsia (PE), hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome, or in patients receiving anti-vascular endothelial growth factor (VEGF) therapy. Excessive soluble fms-like tyrosine kinase 1 (sFlt1) that antagonizes VEGF has been implicated in the pathogenesis of PE. VEGF increases the expression of endothelial nitric oxide synthase (eNOS) and activates it. eNOS polymorphisms that cause reduced NO production are associated with PE. The aim of this study was to clarify the role on hepatic function by excess sFlt1 in the absence of eNOS gene product. We first overexpressed sFlt1 using adenovirus in eNOS

Indexed as

AnimalsBiomarkersDisease Models, AnimalHypoxiaLipid MetabolismLiver DiseasesLiver Function TestsMiceMice, KnockoutNitric OxideNitric Oxide Synthase Type IIIOxidative StressThrombocytopeniaVascular Endothelial Growth Factor Receptor-1BiomarkersNitric OxideNitric Oxide Synthase Type IIIVascular Endothelial Growth Factor Receptor-1

Identifiers

PMID29311569
PMCPMC5758763
OpenAlexW2782162466

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.